Mood Disorders

What was the "bereavement exclusion." What were the reasons for removing this exclusion from the DSM-5 diagnosis of MDD? Discuss some of the criticisms of this change and the reasons why it may prove to be problematic.

-DSM III & IV stipulated that MDD shouldn't be diagnosed w/in 2 months of the death of a loved one unless severe symptoms present (e.g. psychotic features, active suicidal ideation) -DSM 5 decided to remove this exclusion b/c: ~We don't have an exclusion for divorce, break-ups, or job loss - why is there one for bereavement when other forms of loss don't have an exclusion? ~Individuals in need of treatment are often overlooked >Framing bereavement as a diagnosable medical condition may decrease stigma & identify those who need treatment >By receiving a diagnosis w/in 2 months of their loss, ppl might receive more immediate & appropriate treatment >Some research indicates that SSRIs may be helpful w/ bereavement ~Bereavement-related depression & MDD present w/ similar symptoms (e.g. anhedonia & depressed mood) -Criticisms of this change include: ~May pathologize & stigmatize normal grief ~People experiencing loss will unnecessarily be diagnosed w/ MDD even though can have differing course & outcomes >Not associated w/ increased recurrence of MDD >Likely to remit spontaneously (more transient & context-dependent) >Shorter duration of depressive symptoms >Fewer suicidal symptoms -May prove to be problematic b/c: ~Could increase heterogeneity of MDD (problematic for research) ~Now more likely to medicate grief -Persistent complex bereavement disorder proposed as a condition for further study in the DSM 5 (must have at least 6 symptoms of reactive distress at least 12 months after the death

h) Hopelessness theory

Abramson, Metalsky, & Alloy (1989) "expectation that highly desired outcomes won't occur or that highly aversive outcomes will occur and that one can't change this situation-hopelessness-is the proximal sufficient cause of hopelessness depression" Re-re-revised learned helplessness, not that different from the last revision Negative inferential styles of negative events: Attributed to stable and global causes lead to other negative consequences Due to negative self-characteristics (person is unworthy) Whichever inferential style is most vulnerable will lead to the depression These negative inferential styles are used to process negative events, resulting in hopeless depression

Revised learned helplessness theory

Abramson, Seligman, & Teasdale (1978) - After Beck Reason for revision: Failure of the original model to distinguish personal and universal helplessness - few people would become depressed if they failed a test that everyone fails This alleviates helplessness because how you think about it must make a difference Did not address issues of generality and chronicity When and why does a person generalize beyond the helpless situation? Studies in which subjects did not generalize from one experiment to the next (Unsolvable anagrams) o Reactance (Wortman & Brehm) → group of people who wouldn't get helpless, instead they would try harder o Uncontrollability is not sufficient for depression (probability of a positive outcome must be low or of a negative outcome high) § Don't become depressed after uncontrollable positive event § This involves how you make sense of the events you partake in Attributions for negative events - how people explain the negative events, not just the noncontingent punishment Internal vs external (self) global vs specific (world) stable vs unstabltgggggggggggdbe (future) Essentially Beck's cognitive triad Evidence for: ASQ (I think attributional style questionnaire?) Measures attributional style High month test-retest reliability can predict depression following failing midterms (Metalsky) linked to traumatic accidents in college CAVE (interviews) and diaries looking at attributional styles show very stable correlations over time

Discuss the evidence for G x E interactions in the etiology of unipolar model disorders (especially with respect to cognitive/attentional biases in depression). What is the evidence for G x E x Cognition interactions in depression? Discuss the evidence that cognitive/attentional biases may serve as endophenotypes for depression.

Cognitive/attentional biases in depression Depression involves biases toward stimuli conveying sadness and loss​ anxiety toward threat Kids with more 5-HTTLPR S with negative attributional styles have a stronger connection between maternal criticism and child depression Depressed individuals have cognitive biases that essentially make it difficult to not focus on negative information around them Genetic risks for depressive disorders most likely to be expressed in high stress environments Those with certain genetic predispositions like 5-HTTLPR S allele have stronger amygdala reaction to stress, stronger cortisol response, greater attention to threat/anxiety triggers, and higher likelihood to ruminate on emotional stimuli. Those with long allele seem to experience opposite of some of these tendencies When place in certain environments (depressed or angry mothers), it seems these genetic predispositions interact to reinforce these attentional and rumination biases stated above. G x E x Cognition: 5-HTTLPR S allele having children with negative attributional biases have depression levels closely related to mother's depression levels. Basically, it looks like genetic variations that screw with serotonin reuptake, NE, and DA may affect cognitive biases in high stress environments.

Coyne's interpersonal

Coyne (1976), student of Lewinsohn People with depression don't just believe they're socially aversive, they actually are They see the world as it actually is and people don't like to be around them Depressed people are overly realistic, makes them socially aversive and people dislike/avoid them Others attempt to "help" but can't, so they abandon the depressed person Positive feedback cycle: Depressed seeks reassurance -> other attempts to reassure, not well -> depressed recognizes this failure, perceives ambivalence -> repeat (positive feedback cycle) Depressed people often rejected by significant others Supporting evidence: Depression and the Response of Others - Coyne (1976) Had subjects talk with depressed patient, non-depressed patient, or control on phone. Social Skills (Joiner, 2002) Depression associated with poor social skills - observers rate depressed individuals as having poorer social skills, but depressed people rate themselves more harshly Depressed people speak more slowly, with less volume and longer pauses, take longer to respond when others talk to them - voices of depressed people are rated more negatively Negativity in social interaction more likely among acquaintances and intimates than with strangers Depressed people are more self-focused Showing environmental social factors may have a role in maintaining depressive behaviors. Also showed talking to depressed people made subjects feel depressed. "The depressed patients induced negative affect in those with whom they interacted and were rejected."

Bipolar (and all subdisorders like type 1, type 2, cyclothymia, etc.) epidemiology, symptoms, DSM 5 criteria, course, comorbidity, etc.

DSM 5 manic episode must last at least a week (less if hospitalized) A. district period of abnormally/persistantly elevated, expansive or irritable mood and increased goal directed activity or energy B. 3 of 7 symptoms (4 if just irritable mood) 1. inflated self-esteem or grandiosity 2. decreased need for sleep (feels rested even after little sleep) 3. more talkative 4. racing thoughts, flights of ideas 5. Distractibility 6. increase in goal directed activity 7. excessive involvement in pleasurable experiences with potential painful consequences (ex: shopping spree) C. Must cause severe impairment or hospitalization what differentiates mania from hypomania hypomanic episode A. and B. are the same as manic episode C. unequivocal change in functioning that is uncharacteristic of the individual when not symptomatic D. the disturbance is visible by others E. not severe enough for hospitalization and marked impairment difficult to distinguish Bipolar I Must have at least 1 manic episode​ unipolar mania is rare in clinical settings but common in community studies (25-33%)​ unclear whether this is stable or develops into bipolar mania and depression​ Indicate whether single manic episode, or nature of the most recent episode​ After one manic episode odds of a 2nd are 90%​ 60% of manic episodes precede a depressive episode Bipolar II MDE + hypomanic episode​ According to DSM 5, not a milder version of Bipolar I​ more severe/longer depressive episodes than Bipolar I​ similar rate of suicide attempts as Bipolar I, but higher lethality​ severe role impairment Cyclothymia 2 yrs subclinical hypomanic symptoms + subclinical depressive symptoms​ change from DSM IV which allowed hypomanic episodes​ patients with hypomanic episodes + dysthymia will now be diagnosed with dythymia and "other specified bipolar and related disorder (hypomanic episode without prior MDE)​ Equal sex ratio, but women are more likely to present in clinical settings​ Age of onset adolescence or early adulthood Epidemiology Lifetime prevalence of BD I about 1%, BD II about 1%, sub-threshold 2.4%.​ Most common in the US​ Equal sex ratio BD I (& probably II)​ women more likely to be depressed, experience rapid cycling or mixed state​ higher rate of women presenting for treatment for BD II ​ BD 6th leading cause of disability worldwide (physical & psych) ​ Despite earlier reports, BD is higher in low SES groups​ But rates are higher in high income countries​ Yet BD is also associated with high levels of creatively and accomplishment (found in family members of BD proband). Comorbidity BP is highly comorbid​ 95% have another DSM disorder, and 70% have a history of at least 3 other disorders​ ADHD, ODD, panic disorder, substance use are the most common​ Much of the substance use during the manic phase, while disinhibited. ​ Does childhood BD develop into adult BD? ​ Should irritability and aggression count as symptoms of mania in children? ​ Manic symptoms may not be specific to BD and may be confused with ADHD or CD. ​ BP is also comorbid with metabolic syndrome, heart disease, hypertension, and migraine​ Is there a bipolar spectrum or is it a taxonic condition? Course Age of onset 18 for BP I, 20 for BP II​ younger than for MDD​ Onset < 17, increased risk of rapid cycling​ Age of onset getting younger across cohorts​ 1 in 3 pts with cyclothymia eventually develops BD​ About 20% of BP pts in therapy are rapid cycling​ Depressive symptoms persist longer than manic​ Bipolar 1 3:1 ratio of depressed to manic episodes; bipolar II 37:1 depressed to hypomanic​ Subsyndromal symptoms are present over ½ the time the pt is not in an episode​ Over a 5 yr period about ¾ of pts have recurrences (even if medicated)​ If untreated, BD generally gets worse​ Also the longer untreated the less responsive to Li​ Higher daytime motor activity on Li, predicts relapse

What brain regions/structures have been implicated in mood disorders? What is the evidence for these regions?

Depression -Hyperactivation of the amygdala ~Increased subjective experience of emotion, emotional reaction to stimuli, remembering emotional events -Hyperactivation of subgenual anterior cingulate cortex ~Involved in emotion regulation -Hypoactivation of the Dorsolateral PreFrontal Cortex ~Regulates emotion ~Diminishes amygdala activity (back to first bullet point) Bipolar Disorder -Involves emotional control circuit (i.e. increased arousal coming from amygdala & prefrontal cortex not inhibiting correctly) → too much emotion (us rn) ~Doesn't involve the areas of the brain atrophy found in SZ or the cognitive deficits ~Elevated amygdala activity & large volume >Amygdala causes increased emotional sensitivity ~Diminished executive structures are less capable regulating the emotional response (due to less activity) ~Diminished hippocampus & prefrontal activity >Diminished anterior cingulate activity during mania (frontal activity that would lead to inhibition & self-control) ~Hyperactivity in the basal ganglia during mania may result in increased reward motivation -BAS (behavioral activation system) associated w/ dopaminergic systems that run from the ventral tegmental area to the (left) frontal cortex, esp the dorsomedial PFC, ACC, orbitofrontal cortex, & DLPFC ~Mania associated w/ increased left PFC activity & depression w/ right

Unipolar depressive disorders are far more common in women than men. What are some possible reasons for this sex difference? This sex difference only emerges in adolescence. What are some reasons for this emerging sex difference that have received empirical support?

Depression is twice as common in women as in men. Potential reasons: Hormonal factors Women more likely to live below the poverty line, poverty increases risk for depression Women more likely to experience traumatic events, particularly physical and sexual abuse, which increases risk for depression; genetically-depression runs in families more so for female members Women have more first onsets But recurrence rates and durations are equal At 12-13 rate increases sharply in girls, but remains constant in boys This is about the time girls go through puberty, hormonal and psychosocial factors Psychosocial factors Stressful events during this time raise the risk of depression Girls are more likely to have become depressed if they go through peak pubertal changes several months before their peers Also more likely to end up in an inappropriate relationship (older boyfriend) Kids who have been sexually abused go through puberty earlier Increased rates of anxiety d/o, EDs, substance abuse, and delinquent behavior Girls are more likely to dislike the physical changes that come with puberty Hormonal factors Normal hormonal changes aren't associated with significant mood changes Premenstrual dysphoric disorder may be a risk, but only for a small percentage Postpartum depression Most had history of depression Postpartum depressed women similar to other depressed women in past psychiatric history, course of the episode, and psychosocial variables during episode (interpersonal conflict, etc.) Gender differences in rumination, most convincing empirical evidence!! (Susan Nolen-Hoeksema) Rumination is focusing on one's symptoms of distress and the possible causes and consequences of these symptoms in a repetitive and passive manner Rumination predicts the onset of depression People who ruminate have longer periods of depressive symptoms and more intense symptoms, more likely to relapse Associated with increased amygdala activity Women ruminate more than men, possibly due to socialization When rumination is controlled for, the gender difference in depression becomes non-significant!!! But there may be issues with these findings: rumination measurement questions overlap a lot with depression measurement questions

Seligman's original learned helplessness theory

Depression results from noncontingent punishment Outcomes are perceived to be independent of behavior No control over punishmentà learned helplessnessàdepression Give up when perceive an adverse situation won't change no matter what you do The two dog experiments (1960s): Phase 1: Two harnessed dogs. Both of them are receiving shocks, but only one dog has access to the control that controls the shocks. Phase 2: Dogs are now placed in a condition where the shock is avoidable by jumping over a small barrier. The dog who had access to the button in phase 1 will avoid the shocks, the dog who did not have access to the button will not try to avoid the shocks. Dogs that were not helpless were removed from data analysis

What neurotransmitters have been implicated in mood disorders? What is the permissive hypothesis? What is the evidence for the involvement of these neurotransmitters?

Depressive Disorders Neurotransmitters implicated in unipolar depression: NE, DA, 5-HT original focus on NE: MAOI's can be effective but lethal- prevent MAO (monamine oxidase) from breaking down NE (5-HT and DA), which increases levels of NE at the synapse Permissive hypothesis: low levels of 5-HT permit variations in other neurotransmitters to have a greater effect on mood; low 5-HT plus low DA or NE leads to depression Evidence for involvement: effectiveness of MAOIs and SSRIs (which prevent the reuptake of serotonin, thereby raising 5-HT levels) low levels of 5-HIAA (a 5-HT metabolite) in MDD patients milkshake with amino acids experiment- reduction in 5-HT- leads to symptom return in those with MDD history and 1st degree relatives but little effects on subjects without a history or family history of depression Acute tryptophan depletion- tryptophan Other amino acids are inhibiting the production of trytophan (which is implicated in the process of making 5-HT) Bipolar Disorders Neurotransmitters implicated in bipolar disorder: serotonin (5-HT), dopamine (DA), norepinephrine (NE), glutamate Permissive hypothesis: (BD): low 5-HT permits greater fluctuations in DA levels (maybe NE too) Evidence for involvement: greater reward sensitivity in mania (involves DA); increased DA sensitivity in BD (amphetamines and sleep deprivation can trigger mania in people with BD; elevated glutamate levels in prefrontal cortex; decreased serotonin sensitivity; increased DA may be related to mania -neurotransmitter dysfunction is similar in MD and BD Significance of serotonin as a neurotransmitter in BD- giving a BD individual SSRIs causes adverse effects

Describe the BAS dysregulation model of mania. What is the evidence that supports this model?

Depue proposed a BAS dysregulation model in the 80s (Behavioral Activation System) Individuals with Bipolar have high BAS self-report scores (even when not manic) Drive, Fun Seeking Also, Sensitivity to Reward Scale BAS scores predict first onset of Bipolar and transition from Bipolar II to Bipolar I BAS activation associated with high activity, exploration, goal seeking, Positive Affect, etc. BAS activated high outcome expectancy, euphoria low outcome expectancy irritability, anger, violent behavior Mania is associated with more ambitious/unrealistic goal setting (which is then related to a worse course of mania) Scores on the WASSUP popular fame and financial success scales (next slide) predict increases in mania in people with bipolar Also with expending greater energy in the pursuit of goals Also, continuing at tasks that have a lower probability of success Low BAS associated with low motivation, lack of PA, hopelessness, etc. The BAS regulates approach motivation and goal-directed behavior to attain rewards. It is activated by rewards or goal-relevant cues, which can be either external (presence of a desired goal) or internal (expectancies of goal attainment). BAS activation is implicated in the generation of positive goal-striving emotions such as happiness. Recent work also documents an association between anger and BAS activation when goal striving is frustrated. The BAS has been linked to a reward-sensitive neural network, which involves dopamine neurons that project between several emotion- and reward-relevant limbic and cortical brain systems . According to the BAS-dysregulation model, vulnerability to bipolar disorder is reflected in an overly sensitive BAS that is hyperreactive to relevant cues. Such trait BAS hypersensitivity leads individuals to experience variability in their state levels of BAS activation across situations and over time. When vulnerable individuals experience events involving rewards or goal striving and attainment, their hypersensitive BAS becomes excessively activated. This leads to (hypo)manic symptoms, such as excessive goal-directed behavior, increased energy, decreased need for sleep, optimism, and euphoria. Alternatively, in response to events involving definite failures, losses, or non-attainment of goals, a hypersensitive BAS becomes excessively deactivated, leading to a shutdown of behavioral approach. Consequently, depressive symptoms such as decreased goal-directed activity, decreased energy, loss of interest, hopelessness, and sadness result

What is the evidence for a genetic component to unipolar mood disorders? Considering this evidence, how might unipolar mood disorders be transmitted genetically? What is the evidence that Bipolar disorder has a genetic component?

Evidence for unipolar mood disorders be transmitted genetically: Depression runs in families, especially for female members Heritability roughly 40% - 50% Higher heritability in relatives of probands with recurrent cases of MDD than for single episode Also higher in adolescent onset depression than adult onset Strong genetic ties between MDD and GAD (not with other anxiety disorders). The diathesis may be for negative affect/neuroticism. Environmental factors may explain whether the person develops MDD or GAD. Twin Study: Depression concordance rates: Identical twins (.36); Fraternal twins (.17) 2. How might unipolar mood disorders be transmitted genetically: Lau & Eley (2010): "quantitative trait loci" (QTL): multiple susceptibility genes each contributing a small effect Linkage studies: A genetic marker is a sequence of DNA more prevalent among affected family members than among unaffected family members marker could be the disease gene or it could be near the disease gene. Association studies: Compare genetic markers in unrelated samples who either have or don't have the condition Focus on genes that are believed to affect the neuropathology of the disorder Failure to replicate seems to be the rule. 5HTTLPR (Serotonin transporter gene), which is involved in serotonin reuptake has been the most studied, with mixed results Oddly the short variant has been implicated in depression, but that variant results in less reuptake, more 5-HT in the synapse "it is the low-activity short variant of 5HTTLPR that is associated with risk for depression. Lower activity implies fewer transporter molecules at the synapse, which by inference should result in higher levels of serotonin." (L&E, 2010) Brain-derived neurotrophic factor (BDNF) promotes neural growth and prevents atrophy. The allele associated with reduced BDNF levels has also been implicated in depression again with mixed results The DRD4.2 gene, which is associated with DA has also been implicate 3. Evidence that Bipolar disorder has a genetic component: Bipolar disorder has higher heritability than unipolar depression (or schizophrenia). Approx 85% heritability. Concordance rates seems to vary across studies, but MZ twins generally 4-5x greater concordance than DZ twins Being related to a person with bipolar disorder raises risk of developing any type of mood disorder more 1st degree relatives of bipolar individuals have unipolar depression than bipolar. Shared genetic vulnerability between bipolar and SZ, possibly due to a gene involved in DA metabolism. MZ twins of proband with schizophrenia have 8% risk of mania MZ twins of proband with mania have a 14% risk of schizophrenia Twin Study: Bipolar: Identical twins (.80); Fraternal twins (.16)

Lewinsohn's original behavior model

Ferster (1965), Lewinsohn (1974) Depression results from lack of positive reinforcement from the environment Possible reasons for this: Impoverished environment with generally few enforcers (supermax prison). When there is no positive reinforcement, person stops emitting behaviors Both number of reinforcing activities individual engages in, and the amount of positive reinforcers the environment can provide Lacking of social skills results in behavior not being reinforced, or even punished Later revised to throw in a cognitive component, kinda defeated the point Excessive self-focus, self-criticism, pessimism, gulf between standards and accomplishments Some empirical support. Multiple studies looking at social/interpersonal behaviors of depressed individual Lewinsohn & Libet, 1972 social activities negatively correlated to depressed mood Behavioral activation therapy increases opportunities for reinforcement and can effectively lower depression in some individuals ex) person who was not leaving the house and engaging with people joins a bowling league. Has an opportunity to leave house and have fun every week. Makes friends and has positive social interactions. Starts going to other activities with these friends? (I don't actually know I'm not a therapist)

A client comes to see you who you suspect may have a bipolar or related disorder. What questions would you ask her? What questions would you ask to differentiate among bipolar I, bipolar II, and cyclothymic disorder? What would you need to know to determine if she was rapid cycling? If the client were delusional when she came to see you, how would you differentiate between Bipolar I with Psychotic Features and Schizoaffective Disorder?

First, confirm that a manic or hypomanic episode is occurring or has occurred: Are you experiencing or have you experienced a distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal-directed activity or energy? If so, how long has/did this period last? Must be at least 1 week (unless hospitalized) "Do [or have] you experience[d]... Inflated self-esteem or grandiosity? Decreased need for sleep? Increased talkativeness or pressure to keep talking? Flight of ideas or feel as though your thoughts are racing? Distractibility (i.e., attention too easily drawn to unimportant or irrelevant items)? Increased goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation? Excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments)? NOTE: *3+ of these must be answered in the affirmative; 4+ if they are only experiencing irritable mood Next, evaluate the severity of her impairment If impairment is severe (lost job, divorce, bankruptcy, etc.) or hospitalization was required, this would qualify as a manic episode and bipolar I would be the diagnosis Unipolar mania is rare but can occur and is sufficient for a BP I diagnosis If impairment is not as severe, then ask: Have you experienced an unequivocal change in functioning that is uncharacteristic of you under normal (non-symptomatic) circumstances? Are these disturbances of yours visible by others? If these are answered in the affirmative, the client can be considered to have experienced hypomania at a clinically-significant level. If not, could be considered presenting with subclinical hypomania Now must confirm that a major depressive episode (MDE) is occurring or has occurred If so, and we previously determined that the client experienced hypomania, bipolar II would be the diagnosis If no true MDE experienced and just dysthymia, AND the client experienced hypomania, diagnosis would likely be "other specified bipolar and related disorder" (hypomanic episode without prior MDE) How many distinct episodes of mania/hypomania and/or depression have you experienced in the past year? If 4+ episodes, would qualify as rapid cycling (for either BP I or BP II) Can be full remission (back to back depressive or manic episodes between remission period) or switch to opposite pole If the client presented with both subclinical hypomania and subclinical depressive symptoms, ask, "How long have you been experiencing [these subclinical symptoms]?" If 2+ years, can diagnose with cyclothymia If she does not experience delusions or hallucinations that DO NOT occur for at least 2 weeks in the absence of mood disorder, AND the client meets aforementioned criteria for BP I, diagnose as BP I with psychotic features (and not schizoaffective disorder)

What role does the HPA axis & the endocrine system play in mood disorders and what is the evidence? Be sure to discuss the findings from the DST.

HPA axis: Hypothalamic Pituitary Adrenal Axis Stress -- hypothalamus releases Corticotropin-releasing hormone (CRH)--pituitary gland releases Adrenocorticotropic hormone (ACTH) -- adrenal gland releases cortisol Chronically elevated cortisol levels reduce 5-HT function Chronic HPA activation can be neurotoxic, affecting the prefrontal cortex & the amygdala. Cytokines may contribute to the overproduction of cortisol by leading to HPA hyperactivity (disrupting the negative feedback cycle). Dexamethasone suppresses the release of ACTH, which lowers cortisol Many (about 80%) depressed pts. do not have reduced cortisol levels after DST (Dexamethazone Suppression Test) DST: The dexamethasone suppression test is used to assess adrenal gland function by measuring how cortisol levels change in response to an injection of dexamethasone. After you take a dose of it, your body should make less cortisol. That's the idea behind the test -- take some dexamethasone and see whether your cortisol level drops. It is typically used to diagnose Cushing's syndrome → don't have normal response, should lower cortisol especially those with psychotic depression or more severe depression but not specific to depression Remitted pts. with abnormal DST responses are more likely to relapse Children of depressed mothers are more likely to show excessive cortisol levels following a lab-based stressor. HPA axis activation is common in depressed patients. Frequently reported findings include elevated cortisol and corticotropin-releasing hormone (CRH), nonsuppression on the dexamethasone suppression test, a blunted adrenocorticotropic hormone (ACTH) response to CRH, and hippocampal volume reduction. Evidence of HPA axis activation appears to have prognostic value and is associated with increased risk of depression relapse and even suicide.

What does Hammen mean by "stress generation" and how is it related to depression? Discuss the evidence that stress generation plays a role in maintain depression.

Hammen: Depressive people cause stressful life events + create/select adverse environments that heighten the probability of continuing acute and chronic stress Teens with histories of depression, compared to nondepressed youth, more frequently select romantic partnerships in which severe interpersonal violence occurs or elect to give birth before age 20, typically without a job or partner (Hammen et al. 2011, Keenan-Miller et al. 2007) Predictors of Stress Generation: Cognitive vulnerability (e.g. negative cognitive style) Child abuse Attachment insecurity Neuroticism Relational style (e.g. reassurance seeking) Genetic; G x E How does Stress Generation play a role: it predicts a continuing cycle of depression-stress-depression that largely ensures chronic or recurrent depression continuing patterns of depression predicting stress lead to long-term continuity of stress exposure and accumulated stress burden or allostatic load stress generation exposes others in the family to high levels of stressors → conflicts

Beck's cognitive theory

If you aren't depressed, you see the world as it is VS If you are depressed, you see things through a "depressed schema" Schemas result from early childhood experiences Three components in model (CMC book): negative self-statements, cognitive errors, underlying schemas or core beliefs Negative cognitive triad: Negative views of self -> world -> future Cognitive distortions/biases: All-or-nothing thinking - "I won second place. I'm a failure." Catastrophizing - "That email had a typo, they'll fire me for sure" Magnification/Minimization - "One guy reviewed the play badly, we sucked" Driven by schemas AND reinforce schemas Automatic thoughts: consistently depressive and negative (self, world, future) Beck's theories grew from observations of depressed patients personally evaluating self with negative bias. Whole bunch of empirical support. Like 40 years of articles. Studies found people who are depressed/formerly depressed have a cognitive bias for negative words

Discuss the role of the immune system, stress, and social rejection/isolation in the development of depression. Be sure to discuss the role of cytokines in your answer. What is the evidence that the immune system may play a role in depression?

Immune system has 2 branches (Adaptive immunity: white blood cells that respond to specific microbes; takes days to develop) Innate immunity: designed to respond quickly to injury or infection; release cytokines that trigger inflammatory processes to aid healing When activated, the innate immune system releases cytokines that trigger inflammation to help with healing System wide effects of increased cytokines include, fever, increased heart rate, social-behavioral withdrawal, "sickness behavior" (staying in bed, lethargic, etc.) Chronic inflammation can contribute to diabetes, heart disease, some cancers, AD, etc. Many of these disorders are comorbid with depression! Depressed individuals have higher levels of circulating cytokines Cytokines reduce 5-HT by decreasing the availability of tryptophan Threat of injury/infection can prime innate immunity → increase cytokines → trigger inflammatory reaction Speeds wound healing and combats extracellular infection (bacterial) BUT suppresses defenses against intracellular pathogens (viruses) Evolved for physical threats, but generalized to social threats such as rejection or exclusion Rejection during cyberball can trigger inflammatory response Social rejection triggers pain-related neural systems Early life stress can result in chronic elevated inflammation Social isolation and depression raises inflammation IFN-α (a cytokine) treatment for cancer or hepatitis increases neuro-vegetative symptoms of depression For people with a history of depression also increases the cognitive and affective symptoms Anti-inflammatory medications may reduce depression in a subset of depressed individuals Healthy young adults who took acetaminophen twice a day for 3 weeks reported fewer hurt feelings and were less sensitive to rejection in Cyberball CBT may reduce inflammation HPA axis "fight or flight" reaction is also activated by these social threats Releases cortisol (which also reduces 5-HT function) Cytokines may be making this HPA reaction even more likely to occur Summary: Innate immune system views social threats/attacks as they would physical ones and releases cytokines in response. Cytokines then prompt inflammation in the body to "fight" these threats. Chronic inflammation from cytokine reaction interferes with important neurotransmitters (5-HT) and bodily functions, and may feed into depressive symptoms. HPA axis "fight or flight" reaction also may be aggravated by cytokines. This process may become a positive-feedback loop where this cytokine-inflammatory response is either resulting in, reinforcing, and/or causing relapses in depression symptoms. Bad immune system, naughty cytokines Stay away from david

Depression (and all subdisorders like MDD, PDD, etc.) epidemiology, symptoms, DSM 5 criteria, course, comorbidity, etc.

Major Depressive Disorder (MDD) DSM-5: 5 out of 9 symptoms. symptoms present most of the day for at least 2 weeks. must have dysphoric(depressive) mood or anhedonia remaining criteria are related to changes in behavior 1. Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feeling sad or empty) or observation made by others (e.g., appears tearful). (In children and adolescents, this may be characterized as an irritable mood.) 2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day 3. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day. loss of appetite more common 4. Insomnia (inability to sleep) or hypersomnia (sleeping too much) nearly every day insomnia more common 5. Psychomotor agitation or retardation nearly every day 6. Fatigue or loss of energy nearly every day 7. Feelings of worthlessness or excessive or inappropriate guilt nearly every day 8. Diminished ability to think or concentrate, or indecisiveness, nearly every day 9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide Course 60% of those who had a MDE will have at least one more 70% of those who have 2 will have a 3rd; 90% of those with 3 will have a 4th 54% of MD pts recover w/I 6 months, 70% w/I a year; 88% w/I 5 yrs, 93% at 10 years 22% relapse within 1 year-predictors of relapse Multiple prior episodes Older age History of non-affective psych illness Double depression The typical MDD patient has 4 lifetime episodes each last 20 weeks 20% of MD had episode before 25; 50% before 39 66% remit entirely, 5-10% of MDE can last over 2 years; recovery between episodes is partial for 20-25% of pts; 25% of pts with recurrent MDE develop dysthymia 25-40% chance of recurrence after 2 yrs, 60% after 5 yrs, 75% after 10 yrs, & 87% after 15 yrs Prior episodes increase the risk of recurrence, and shorten the period between episodes. Patients who fully recover have a lower recurrence rate (66%) than those who have residual symptoms (87%). Risk factors for recurrence include, history of prior episodes, double depression, age of onset after 60, long duration of episodes, & family history Comorbidity 75% lifetime comorbidity rate with another psych disorder, 8% one month comorbidity Usually the other disorder precedes depression (especially in men). Anxiety and substance abuse disorders are especially likely to lead to depression. Anxiety disorders--people with MD are: 6X more likely to have GAD 4X panic disorder 4X PTSD Patients with Schizophrenia: 28.5X more likely to become depressed than populations, Panic Disorder: 18.8X more likely to become depressed 56% of anorexics are depressed, 24-33% of bulimics 14.5% of MD & 20.9% of dysthymia have substance abuse problem. Frequently comorbid with medical disorders: 18% of diabetics 22-33% of hospitalized medical patients 18% of myocardial infarctions (but partly may be over diagnosed because of symptom overlap) Comorbidity―Personality Disorders 48-75% of MD patients have a personality disorder 81% of inpatients with depression likely to have personality disorder Ilardi & Craighead (1999)-patients with personality disorder are likely to have depressotypic cognitions (ASQ & DAS) even in the absence of syndromal depression Prevalence Lifetime prevalence of MDD--17% in US 20-25% in women, 9-12% in men Women are 2 times as likely to have a 1st episode, but no sex differences in rates of recurrence (or 1.5-3x according to the textbook) Ethnic variability in the United State: Native Americans (19%), African Americans & Asians (9%), Hispanics (10%) Not great consistency across national surveys, with lifetime prevalence rates ranging from 5-25% prevalence rate increase & onset time become earlier for recent birth cohort Gender difference 2X more in women More 1st onsets Equal rates of recurrence & equal duration Equal in children At age 12-13 rate increases sharply in girls (remains constant in boys) Girls are more likely to become depressed if they go through peak pubertal changes several months before their peers also have increased rates of anxiety disorders, eating disorders, substance abuse, & delinquent behavior Persistent Depressive Disorder Dysthymia + major depressive episode, chronic (DMS IV) -> PDD (DSM 5) DSM-5: Depressed mood for at least 2 years (1 year in children and adolescents) with more days dysthymic than not, and no period more than 2 months without symptoms 2 of 6 other symptoms: Poor appetite or overeating Insomnia or hypersomnia Low energy or fatigue Low self-esteem Poor concentration or difficulty making decisions Feelings of hopelessness Specifiers: With anxious distress With mixed features With melancholic features With atypical features With mood-congruent psychotic features With mood-incongruent psychotic features With peripartum onset Specify dysthymia with persistent Major Depressive Episode(MDE), intermittent MDE, or pure dysthymia (no MDE) Specify early onset (< 21) or late (≥ 21) Specify if in partial remission vs. full remission Specify current severity (Mild, Moderate, Severe) Early onset (< 21) is associated with Greater genetic loading for mood disorders Greater childhood adversity Greater comorbidity More HPA dysregulation Late-onset usually the result of chronic stressful life events Prevalence Lifetime prevalence of PDD 1-6% in US PDD is associated with lower income Roughly 25% of adults have had either MD, minor depression, or recurrent brief depression. Comorbidity Compared to MDD: Higher risk for psychiatric comorbidity in general, and for anxiety disorders and substance use disorders in particular Early onset is strongly associated with DSM-IV cluster B and C personality disorders Course: Early and insidious onset Chronic course In MDE: Go down to a lower level quickly but are less likely to resolve in a given period of time (compared to MDD) Persistent Depressive Disorder Compared to MDD Greater comorbidity anxiety disorders, substance use, personality disorders Lower self-esteem Greater suicidality Greater early adversity More frequent family history of depression Less responsive to therapy more likely to benefit from medication + psychotherapy Risk that PDD may be too heterogeneous chronic MDD is usually very severe, persistent, and treatment-resistant dysthymic disorder is often much milder, not meeting the full criteria for MDD

b) Bibring's psychoanalytic

Mechanisms of Depression (1953) Depression results from state of helplessness Ego experiences helplessness in different ways depending on developmental stage Oral - Dependent Very young, baby - "Help me or I will die" Anal - Self-critical Toddler, toilet training - "I'm I am not toilet trained, I am bad" Beginning of social comparison- meeting developmental milestones Phallic - Unappreciated/excluded Young child - "Why don't I get to stay up late?" Unreciprocated social interactions, beginning to be able to take perspective of others Depression "flavors" come from these developmental stages, themes of depression that can overlap and mix First link to depression and helplessness First discussion of heterogeneity in depression No empirical support

A client comes to see you who you suspect may have a depressive disorder. What questions would you ask her? What questions would you ask to differentiate between persistent depressive disorder and major depression? If it looked like major depression, what questions would you ask to determine if it was Melancholic Type? Atypical Depression? If the client were delusional when she came to see you, how would you differentiate between Major Depression with Psychotic Features and Schizoaffective Disorder?

Meloncholic feature: must include anhedonia, + 3/6 other symptoms. Distinct depressed mood, worse in AM, early morning awakening, psychomotor retardation or agitation, anorexia/weight loss, excess guilt. Atypical Depression: Atypical but not rare ( 15% or MDD patients). Mood reactivity + 2/4 other symptoms. Weight gain, hypersomnia, leaden paralysis, rejection sesitivity. PDD is depression that lasts > 2 years. PDD includes chronic MDD, so PDD not necessarily less severe than MDD. MDD > 2 weeks for Dx. MDD must have 5/9 symptoms and must include either depressed mood or anhedonia. Major depression: Five or more of the following symptoms have been present during the same 2-week period and represent a change from previous functioning. At least one of the symptoms is either depressed mood or loss of interest or pleasure: Depressed mood most of the day, nearly every day, as self-reported or observed by others Diminished interest or pleasure in all or almost all activities most of the day, nearly every day Significant weight loss when not dieting, weight gain, or decrease or increase in appetite nearly every day Insomnia or hypersomnia nearly every day Psychomotor agitation or retardation nearly every day Fatigue or loss of energy nearly every day Feelings of worthlessness or excessive or inappropriate guilt nearly every day Diminished ability to think or concentrate nearly every day Recurrent thoughts of death, recurrent suicidal ideation without a specific plan. In addition, these symptoms: Cause functional impairment (e.g., social, occupational) Are not better explained by substance abuse, medication side effects, or other psychiatric or somatic medical conditions. Persistent depressive disorder This diagnosis encompasses and expands the now-unused diagnosis "dysthymic disorder". The patient has a major depressive syndrome or 3 or 4 dysthymic symptoms, including depressed mood, for ≥2 years. Impairment compared with major depressive disorder may be less severe. Dysthymic symptoms are as follows: Depressed mood Appetite changes Sleep changes Low self-esteem Fatigue Poor concentration Hopelessness. Questions: Mood · Have you felt low or depressed in yourself lately? · Have you felt low/depressed/tearful every day, for most of the day, in the last two weeks? Anhedonia · What are kinds of things that you normally enjoy doing? (Anhedonia) · Have you been enjoying these activities as much as you've done in the past? (Anhedonia) Anergia · Have you been feeling unusually tired in yourself lately? (Anergia) · How have your energy levels been over the past couple of weeks? Concentration/Decision Making · Have you been able to focus on things lately? · What's your concentration like? Appetite · Since you've been feeling low, have you noticed any changes in your appetite? · Since you've been feeling low, have you noticed any changes to your weight? · Has it increased, decreased or stayed the same? Sleep · What has your sleep been like lately? · Do you find it difficult to fall asleep? (Initial insomnia) · Do you find it difficult to stay asleep? (Middle insomnia) Hopelessness, guilt, worthlessness · How do you see the future? Suicide · Have things got so bad, that you feel like life is not worth living? · It is not unusual/sometimes when people feel low they may have thoughts of suicide/not wanting to be here... Have you ever felt that way? For MDD w psychotic features the psychotic features should only be present during a depressive episode where as for Schizoaffective disorder the delusions and hallucinations should persist outside of the affective episode.

I may pick two or three of the following theories of depression and ask you to describe the theories, provide any empirical support for the theories (if applicable), and compare and contrast the theories: Freud's psychoanalytic, Bibring's psychoanalytic, Lewinsohn's original behavior model, Coyne's interpersonal, Seligman's original learned helplessness theory, the revised learned helplessness theory, Beck's cognitive theory, and Hopelessness theory. Freud's psychoanalytic:

Mourning and Melancholia (1917) People with depression have a lot in common with people who are grieving Self-criticism in depression is often internalized anger at another person, seems like it's aimed towards the self, but it's actually aimed towards someone else When someone/something have "lost" energy (libido) that was attached to subject of loss, it has to go somewhere. That negative energy is internalized → Grief When you care for someone, you invest libido (mental energy) in them Withdrawing this (loss) is painful Ambivalent feelings toward lossed target results in aggression being redirected at the ego → self-punishment, criticism No empirical support