1
Affective Disorders Outline
What is a mood disorder?
The etiology of an affective disorder:
1. biological process? What is the evidence?
2. problems with studying biological processes.
3. are biological abnormalities unrelated to the primary disorder?
Biological Theories of Affective Disorders
Familial & Genetic Influences
 Probands 2-3x higher than in normal probands.
 Proband with bipolar disorder – relative has unipolar depression,
not bipolar.
 Adoption studies mixed.
 Twin studies: identical – other twin 3x as likely than fraternal twin
to have mood disorder.
 Sex differences – higher for females.
 Environment – higher role in males.
 Unipolar & bipolar seem to be inherited separately.
Neurological Influences:
 Low levels of serotonin in relation to other neurotransmitters,
including norepinephrine & dopmine.
 Serotonin’s function = to regulate systems involving norepinephrine
& dopamine.
 Permissive Hypothesis – stipulates that where serotonin levels are
low, other NTs are permitted to range more widely, become
dysregulated, and contribute to mood problems.
 Endorine system involvement, e.g. elevated levels of cortisol. The
relationship of dexamethasone suppression test (DST) = less
suppression of cortisol.
 Sleep disturbance – depressed individuals move into REM sleep
more quickly and shows diminished slow wave sleep.
 Bipolar individuals show increased sensitivity to light.
 Different alpha EEG values reported in 2 hemispheres of brains of
depressed individuals.
Is depression similar to the common cold?
The history of depression
 Disruptions of balance among four fluids or humors in the body
 Melancholia = imbalance of black bile.
2



Sadness, a tendency to suicide, feelings of indifference,
psychomotor agitation.
Kant = emotions don’t cause mental illness.
Abraham (1960) & Freud (1917) psychological/emotional factors in
onset & maintenance of depression
Issues with Diagnosis of Mood disorders
 Mood should be separate from melancholia characterized by psychosis or
delirium
 Kraeplein (1904/1968) Mania separate disorder from schizophrenia or
other psychotic disorders.
 Other early theorists did not make this distinction.
 Current evidence: difference in unipolar versus bipolar disorder.
 Other distinctions: endogenous (naturally occurring depression) versus
psychogenic or reactive depression.
 Personality “trait” versus reactive “state”
 Issues of bereavement (Beckham, Leber, & Youll, 1995)
 Dysthmia
 Cyclothymia, bipolar I, bipolar II
 Adjustment disorder with depressed mood
 Major depression
 Cognitive versus biologically mediated depression
 Nonaxious versus anxious depression
Definition Issues
 Mood state
 Classification category
 Depression as a symptom
 Depression as a syndrome
 Categorical conceptualization used by DSM-IV
 Issues of continuum
Epidemiology of Depression
 Prevalence 5 to 44%
 Estimates vary depending on sample/measurement/children versus adults
 Lifetime prevalence 4.9%
 Lifetime rates 17.1%
 Estimates in population between 3 to 5.3%
 20% display chronic course
 sex differences – 2x more frequently with women versus men
 Age: more common in younger versus older adults; highest 25-45.
 First onset 30s to 40s.
 50% before age 40.
 Rates lower for adults over 65.
3




Gender differences don’t start until mid-adolescence; estimates same for
boys and girls.
Not much difference with ethnicity when SES controlled.
Symptom constellations within cultures.
Worldwide, depression problematic.
Models of Depression
 Historically, single causal agents.
 Contemporary approaches are multifactorial and integrative.
Life Events Model
 Problem with self-report checklist methods
 Possible problems with memory / validity of self-reports
 Is negative life events a consequence or a cause?
 Investigator-based assessment procedures, e.g. Shrout et al (1989)
individuals with depression are 2.5x more likely than nondepressed
individuals to have experienced one or more fateful loss events.
 Semistructure interview method (Brown & Harris, 1986) – severe events.
 Finlay-Jones & Brown, 1981 – loss events especially when they involve a
threat to self-identity & self-worth.
 Additive threats, e.g. Vinokur et al (1996).
 Brown & Harris (1989) – 3/4ths of recently depressed individuals
experienced a preceding negative life event. Also, 1/5 individuals went on
to develop depression.
 Women 3x more likely to develop depression.
 Vulnerability factors = low social support & low self-esteem.
 But…women contributory role? Poor interpersonal problem solving?
Behavioral & Interpersonal Models
 Problematic interactions with others.
 Social behaviors of the depressed individual?
Lewinsohn’s Behavioral Model of Depression
 Lewinsohn (1974) – depression is the result of a low rate of responsecontingent positive reinforcement, e.g. initiating a conversation.
 Low rate of behavioral responding.
 Depressive symptoms reinforced by social environment.
 Social skills deficit theory?
 The link to negative life events?
 Depressed individuals feel they are less socially skilled.
 They differ on a variety of social skills.
 They speak differently.
 They are more self-demeaning.
4

But…negative life events do correlate with depression, but are not a
sufficient cause of depression.
Lewinsohn Revised Model
 Depression caused by stressful life events in people with inadequate
coping skills.
 Cognitive changes.
 Behavioral changes.
 Person becomes more negative.
 Behaves less competently socially.
 Vicious Cycle.
Coyne’s Interpersonal Model
 Stressful life events, especially loss of significant relationships, =
depression.
 Goal: restore social support, gain acceptance.
 Friends & family respond with concern & support = reinforces the
depression symptomotology.
 But …. Eventually aversive responding.
 Depressed people are rejected, but features of the person matters.
 Why rejected? Joiner et al (1992); Segrin & Abramson (1994)
Beck’s Cognitive Theory of Depression
 Activation of depressive self-schema.
 This could be relative to a social stressor.
Information-Processing Models of Depression
 Latent structures that have been activated by life event stressors.
 Depressed people think negatively about themselves.
 More critical.
 High recurrence & runs in families.
 Selective encoding of negative information.
 These symptoms disappear when they are not depressed.
 Cognitive distortions? == re-evaluation of Beck’s theory – not inaccuracy
or distorted thought content; negative thought content.
Learned Helplessness (Seligman, 1975)
 Expectations that they are helpless to control aversive outcomes.
 1978 revision – beliefs about the causes of events – attributional style
Abramason et al (1989)
 hopelessness theory of depression
 Separate subtype?
5
Sociotropic & Autonomous Depression Subtypes
 Sociotropic individuals
 Autonomous individuals
Self-regulatory approaches to depression
 How people regulate their behavior in the absence of external
reinforcement.
 The role of cognitive processes.