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.

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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.

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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

response-contingent 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.

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They are more self-demeaning. 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)

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hopelessness theory of depression Separate subtype?

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.

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