Mood Disorders: Etiology

Chapter 6

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

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