Mood Affective Disorders

Mood (affective) disorders are disturbances of mood that go beyond ordinary sadness and impair daily life.

Unipolar vs bipolar.

• Unipolar depression (major depressive disorder) — the mood disturbance is in one direction: persistent low mood.
• Bipolar disorder — mood swings between two poles: episodes of depression and episodes of mania (abnormally elevated mood, high energy, reduced need for sleep, impulsive/risky behaviour).

Diagnosis. As in all clinical work, clinicians match symptoms to DSM-5 (or ICD-11) criteria. For a major depressive episode, a person must show a set number of symptoms (including low mood or loss of interest/pleasure) most of the day, nearly every day, for at least about two weeks, causing significant distress or impairment.

Why reliability and validity matter here too. Low mood is part of everyday life, so the criteria must mark the line between normal sadness and a disorder. Symptoms also overlap with anxiety (comorbidity), and mood is shaped by culture — all of which make valid diagnosis a recurring evaluation point. (See the [[schizophrenia]] note for the general diagnosis framework.)

Symptoms of major depression fall into groups:

• Emotional — persistent low mood, anhedonia (loss of interest/pleasure), worthlessness, guilt.
• Cognitive — poor concentration, indecisiveness, negative thinking, thoughts of death/suicide.
• Behavioural — withdrawal, reduced activity, fatigue / loss of energy.
• Physical (somatic) — changes in sleep (insomnia/hypersomnia), appetite/weight changes, psychomotor changes.

DSM-5 (depression). A diagnosis requires several such symptoms (with low mood or anhedonia as a core), present most of the day, nearly every day, for ~2 weeks, causing impairment, and not better explained by another cause.

Symptoms of mania (in bipolar) are the mirror image: elevated/irritable mood, inflated self-esteem/grandiosity, reduced need for sleep, racing thoughts, distractibility, and risky/impulsive behaviour.

Genetic explanation. Mood disorders run in families: first-degree relatives of sufferers are at higher risk, and twin studies show higher concordance in MZ than DZ twins — suggesting an inherited vulnerability. Concordance is not 100%, so genes set a predisposition that the environment can trigger.

Biochemical explanation (the monoamine hypothesis). Depression is linked to low activity of monoamine neurotransmitters, especially serotonin (and noradrenaline).

• Supporting evidence: drugs that raise serotonin (e.g. SSRIs) reduce depressive symptoms; lowering serotonin can worsen mood.
• In bipolar, dysregulation of these systems is also implicated.

Evaluation in brief. Strong scientific support and effective drug treatments, but reductionist (reduces complex mood to chemistry), and cause vs effect is unclear — low serotonin could be a result of depression, not its cause. The success of SSRIs also doesn't prove a chemical cause (a treatment working doesn't confirm the mechanism).

Beck's cognitive theory. Depression results from negative, distorted thinking:

• The negative triad — automatic negative views of the self, the world and the future.
• Negative schemas (developed early, e.g. through criticism/loss) that bias interpretation.
• Cognitive distortions/biases — e.g. overgeneralisation, catastrophising, selective abstraction. These keep the person trapped in a negative cycle.

Seligman's learned helplessness (and attributional style). From animal studies, Seligman argued that experiencing uncontrollable negative events teaches people they are helpless, so they stop trying. This was extended into a negative attributional style: depressed people tend to attribute bad events to causes that are internal ('my fault'), stable ('it will always be this way') and global ('it affects everything').

Evaluation in brief. Well-supported and the basis of effective therapy (CBT/REBT), but may confuse cause and effect (does negative thinking cause depression, or does depression cause negative thinking?), and can seem to blame the patient for their thoughts.

Biological treatment — antidepressant drugs.

• SSRIs (selective serotonin reuptake inhibitors) block the reuptake of serotonin, increasing its availability and lifting mood. (Older types include tricyclics and MAOIs.)
  • + Effective for many, easy to administer, allow people to function.
  • − Side effects, take weeks to work, treat symptoms not cause, relapse if stopped.

Psychological treatment — CBT (Beck).

• Identifies and challenges negative automatic thoughts and the negative triad, tests them against evidence, and replaces them with realistic thoughts, with behavioural activation (re-engaging in activity).
  • + Tackles the cause (faulty cognition), no physical side effects, lasting benefits.
  • − Requires effort/insight and a motivated patient; less suitable in very severe cases without medication first.

Psychological treatment — REBT (Ellis).

• Rational Emotive Behaviour Therapy uses the ABC model — an Activating event leads to Beliefs (often irrational) which produce emotional Consequences. The therapist disputes irrational beliefs (the D step) to change the emotional outcome.
  • + Directly targets irrational beliefs; empowering. − Confrontational style doesn't suit everyone.

Key framing: drugs target biochemistry; CBT/REBT target cognition — and combining drugs with therapy is often most effective.

Pull the threads together for Paper 3 'evaluate / discuss'.

Strengths

• Effective treatments (SSRIs, CBT, REBT) with strong supporting evidence.
• Testable, scientific biological accounts; practical real-world application.

Weaknesses / issues

• Reductionism — biological accounts reduce mood to chemistry; cognitive accounts may ignore biology.
• Cause vs effect — low serotonin / negative thinking may be consequences of depression.
• Blame — cognitive explanations risk blaming patients for their thoughts.

Relevant issues & debates

• Nature vs nurture / diathesis–stress — genetic/biochemical vulnerability interacting with negative life events and learned cognition.
• Reductionism vs holism — biology alone vs a bio-psycho-social view.
• Free will vs determinism — biochemical accounts are more deterministic; cognitive therapy assumes people can change their thinking.
• Application to everyday life — diagnosis and treatment choice in real practice.