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Mood Disorders: Etiology. Chapter 6. Mood Disorders: Familial and Genetic Influences. 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
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Mood Disorders: Etiology Chapter 6
Mood Disorders: Familial and Genetic Influences • 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: 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
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
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
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)
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
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
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