1. Mood Disorders: Etiology Chapter 6

2. Family Studies Rate of mood disorders is high in relatives of probands Relatives of bipolar probands are more likely to have unipolar depression Twin Studies Concordance rates for mood disorders are high in identical twins, highest for bipolar disorder More severe mood disorders have a stronger genetic contribution (.e.g., bipolar) Heritability unlikely related to single gene, but interaction of many genes creates biological vulnerability Mood Disorders: Familial and Genetic Influences

3. Mood Disorders: Neurobiological Influences Neurotransmitters Mood disorders are commonly related to low levels of serotonin (5-HT) and norepinephrine (the “catecholamine hypothesis”) Low levels of serotonin metabolites (5-HIAA) in CSF Effectiveness of antidepressant that act on this system The “permissive hypothesis” and the regulation of other neurotransmitter systems One function of the serotonin system is to regulate other neurotransmitter systems within adaptive bounds, including noradrenergic (norepinephrine) systems Underactive noradrenergic systems  depression Overactive noradrenergic systems  mania

4. Mood Disorders: Neurobiological Influences Endocrine system and “stress hypothesis” Depression may be linked to excess Cortisol (the “stress hormone” Hypothyroidism and Cushing’s Disease Postpartum Depression Dexamethasone Suppression Test (DST) – not supported as specific to depression

5. Mood Disorders: Psychological Influences The Learned Helplessness Theory of Depression Related to lack of perceived control over life events Hopelessness, not just helplessness, may be key to development of depression Learned Helplessness and a Depressive Attributional Style Internal attributions – Negative outcomes are one’s own fault Stable attributions – Believing future negative outcomes will be one’s fault Global attribution – Believing negative events will disrupt many life activities All three domains contribute to a sense of hopelessness

6. Mood Disorders: Psychological Influence Aaron T. Beck’s Cognitive Theory of Depression Depression – A tendency to interpret life events less adaptively Depressed persons engage in cognitive errors Types of Cognitive Errors Arbitrary inference – Overemphasize the negative Overgeneralization – Generalize negatives to all aspects of a situation Cognitive Errors and the Depressive Cognitive Triad Think negatively about oneself (incompetent, unattractive, etc.) Think negatively about the world (dangerous, cold, etc.) Think negatively about the future (unchanging, painful, etc.) Negative Schema (things are usually my fault)

7. Mood Disorders: Social and Cultural Dimensions Social Support Extent of social support is related to depression Lack of social support predicts later onset of depression Interpersonal theory of depression hypothesizes that cause of depression is strain or loss in interpersonal relationships, alienation from social world Substantial social support predicts recovery from depression

8. Integrative Model of Mood Disorders Shared Biological Vulnerability Overactive neurobiological response to stress Exposure to Stress Activates hormones that affect neurotransmitter systems Turns on certain genes Affects circadian rhythms Activates dormant psychological vulnerabilities (i.e., negative thinking) Contributes to sense of uncontrollability Fosters a sense of helplessness and hopelessness Social and Interpersonal Relationships/Support are Moderators

9. Challenges to Understanding Etiology Diagnostic ambiguity – one disorder or many? Distinct from anxiety? Complex interactivity of biological influences Endocrine responses and genetic expression Interaction of endocrine and neurotransmitter systems Interaction of different neurotransmitter systems Acute vs. delayed responses to biological interventions Cause vs. effect