PSYC 300 Final

• Major Depressive Disorder (MDD)


  • Sad, depressed mood (intense)
  • Loss of interest/pleasure (anhedonia - do not care anymore, lack drive to do things you used to like to do)
  • Sleep difficulties (more or less)
  • Lethargy (lack of energy) or agitation (more physiological energy)
  • Appetite problems / weight loss or gain
  • Loss of sexual desire
  • Extreme fatigue (not the fatigue where you want to take a nap → a level of fatigue where it is hard to get out of bed, brush your teeth, hard to do anything to help yourself, etc.)
  • Feelings of worthlessness and guilt (common and prevalent)
  • Difficulty concentrating
  • Recurrent thoughts of death or suicide
• Inversely related to SES
• Prevalence of MDD


  • Lifetime: ~11%
  • 1-year: ~4.5%
  • ~ 80% experience 1 episode → more (will experience at least one more)
  • Average # of episodes: 4
• Kindling hypothesis


  • Each depressive episode provides more kindling for the next depressive episode
  • More depressive episodes you have had, the easier it is to fall into another major depressive episode when something goes wrong
• • Average duration of MDD: 3-5 months
  • 12% of episodes last > 2 years
  • Gender ratio is 2:1 (women : men)
  • Emerges by mid-adolescence → maintained across the lifespan
  • In childhood it is still present, but it is an equal ratio
  • Chronic MDD is associated with serious childhood family problems and an anxious personality in childhood
• Persistent Depressive Disorder (PDD)


  • Chronic (≥ 2 years) low-grade depression (light depression)
  • Average duration 4-5 years
  • Intermittent normal moods
  • Different from MDD - do not need to have as many symptoms for this
• "Double depression"


  • Frequent periods of MDD superimposed on PDD
  • MDD + PDD co-occurring in the same person
• MDD vs PDD


  • PDD - not as intense low mood, but chronic up and down moods (low-grade depression)
  • "Double Depression" - Do not go back to normal → go back to PDD (do not reach baseline levels)

  
• • Heritability estimate of MDD is ~35%
  • 1st degree relatives 3x higher risk MDD
• Depressogenic reaction to stress

  When people are stressed, they are more likely to react a certain way (more likely to cause/more vulnerable to developing depression)
• 1. HTT alleles


  • Dysfunction in 5-HT system → serotonin is not functioning as well or as effectively as it should
  • Linked to temperament (neuroticism)
  • Hyperresponsive to aversive stimuli and stress
  • Vulnerability for depression and anxiety (why they are comorbid disorders)
  • Short allele (s)
  • Long allele (l)
• Neurotransmitters in MDD


  • Sad, depressed mood (obsessive grief – not like OCD) – 5-HT (decrease)
  • Loss of interest/pleasure – DA (dopamine → decrease)
  • Psychomotor retardation – NE (decrease) → norepinephrine
  • Feelings of worthlessness and guilt (obsessive) – 5-HT (decrease)
  • Recurrent thoughts of death or suicide – 5-HT (decrease)
• "Permissive theory"


  • 5-HT regulates other NTs (ie. NE and DA) → 5-HT does this – the "boss"
  • Decrease NE & DA → depression
  • Increase NE & DA (hyperfunctioning) → mania
• Tryptophan


  • 5-HT precursor
  • Depletion → relapse (people tend to have another depressive episode)
  • Only obtained from food
  • After tryptophan is consumed, it is converted to serotonin via a series of chemical reactions → people with anorexia nervosa have low levels of 5-HIAA, which is a major metabolite of serotonin
• • NTs return to homeostasis before symptoms improve
  • Decrease metabolite levels not consistently found (more often with suicidal ideation and behaviour)
• HPA axis


  • Increase in cortisol (fight or flight hormone)
  • Negative feedback loop → system tries to maintain homeostasis in body
  • Increase in energy release → "rest and digest" system (parasympathetic nervous system)
• Cortisol Suppression: Faulty Feedback

  • Cortisol feedback loop signal is not as strong compared to "normal" subjects
  • Faulty negative feedback loop → flooded with cortisol
• Depression is associated with activation of the inflammatory response system as evidenced by increased production of proinflammatory cytokines
• Stressful event


  • Precipitate the onset of a major depressive episode
  • 4-5 episodes → depression starts to develop its own cycle (no longer requires SLE to cause depressive episode)
  • Excessive cortisol depletes DA (anhedonia)
• Brain Activity in MDD

  • Decrease left PFC (front of your head) - Approach, emotion regulation, turns off amygdala alarm
  • Increase right PFC - Avoid, inhibit, Negative Nelly
  • Increase amygdala - Fear, fear, fear!
  • Decrease anterior cingulate cortex (ACC) - Error-related rewards & losses (selective attention)
  • Decrease hippocampal volume - Memory & learning, also regulates ACTH
• Disruptions of sleep, circadian rhythm, exposure to sunlight, and inflammatory response system may also play a role in MDD
• Independent life events (ILE)


  SLEs that are independent of the person's behaviour and personality
• Dependent life events


  Events that may have been at least partly generated by the depressed person's behavior or personality (play a stronger role in the onset of major depression than do ILE)

  
• Beck's Cognitive Theory


  • Negative interpretations of situations/events
  • Feelings of depression
  • Reciprocal model (each is increasing the other)

  
• Lack of positivity bias


  • Most people who are not depressed, tend to have a positivity bias (think good things about themselves)
  • Having a slight positivity bias is a protective factor
• Greater accessibility of negative content


  Negative interpretations/thoughts are more readily available/prevalent in people who are more depressed
• Beck's Cognitive Model


  • Diathesis - Formation of dysfunctional beliefs (depressogenic schemas) - negative beliefs that are rigid, extreme, and counterproductive
  • Stressor - What causes the beliefs to be activated
• Negative Cognitive Triad


  Negative thoughts about the self, the world, and the future
• Learned Helplessness


  Lack of perceived control over life events
• Depressive Attributional Style


  • Internal attributions → negative outcomes are one's own fault
  • Stable attributions → future negative outcomes will be one's fault
  • Global attribution → negative events disrupt many life activities (across many domains)
• Hopelessness Theory


  • Sense of hopelessness - no hope for the future (helpless and hopeless)
  • The person believes negative outcomes will continue indefinitely
• Psychoanalytical Theory


  Depression = anger turned inward
• Interpersonal Theories


  • People who are depressed may act in ways that genuinely have a negative effect on others and lead to alienation from their social support network
  • Social support network is both protective and helpful in managing or treating the disorder
• • Evidence for Interpersonal Theories:
  • Poor social networks (all eggs in few baskets)
  • Few positive social behaviours
  • Elicit negative reactions from others
  • Marital discord → hostility and criticism between spouses
  • Insecurity in relationships (ie. frequent reassurance-seeking)
• Gender Ratio


  • Women at genetic risk for depression not only experience more stressful life events but also are more sensitive to them
  • Women have more cortisol naturally
  • Women have more fluctuating estrogen : progesterone ratio
• Rumination is a factor in both anxiety and depression
• Relapse in depression is capable of activating some of the neural circuits that are thought to be involved in the disorder
• The person with depression tend to report being less happy/satisfied
• Insecurity in relationships (ie. frequent reassurance-seeking)
• Frequent reassurance-seeking - negative effect on their social network