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First theory- bio principles. Neurotransmitter serotonin- role in activity of other neurotrans- if low, levels of dopamine (involved motor activity + psychotic symptoms) + noradrenaline (involved psychological arousal) can fluctuate wildly. Normal circumstances- all 3 control arousal and emotion, but imbalance w/ neurotransmitters- cause unipolar.
McNeil + Cimbolic eg noticed sig serotonin by-product absent in cerebrospinal fluid of suicidally dep. Bunney and Davis noticed level of important noradrenalin by-product sig lower in urine of dep than not. suggest link between neurotrans and unipolar, but only correlational- may be the condition itself that causes lower levels rather than vice-versa.
Anti-deps eg MAOI and SSRIs- preventing reuptake of serotonin thus increasing levels. Success rate- 65-75% so could argue levels of serotonin largely implicated in disorder. But 'hello-goodbye' effect, pps overestimate improvement. Also altho affect neuros immediately- lag time 2-6 weeks suggesting other factors sig.
Kennet- drugs work by increasing sensitivity to receptor sites to serotonin explaining lag time. Individual variance in tolerance questions cause of disorder, 2 individuals, same treatment but diff consequences. Suggests factors eg emosh support, even genes, play a role.
Bio seems at least contributory- Delago: giving previously depressed patients a diet low in Tryptophan (known important in creation of serotonin)- found shared depressive symptoms= level of serotonin seems key in uni dep.
Second Theory- genetic- comparing MZ can examine role of genes in dep. McGuffin et al- if 1 twin has uni 46% other will- 20% in DZ. May be that MZ share more same social exp and treated more similarly. Even so role of gen seem contributory. Bio reasons suggest individuals determined to certain cond. MZ 100% genes, but 54% not both deve uni- implies other factors.
Freud- psychodynsmic theory- 3 parts personality: id, ego, superego- define. observed dep like berievement+grief- if lose something in early chikdhood, dep= adult life. Anger of loss internalised= self hatrid result of ego defence mech ineffectively redirecting anxiety inward. These conflicts= uncon until trigger csuses symp.
Shah and Waller (2000) deps describe 'rents as "affectionless" supports F's 'loss' concept- withdrawal of affection. but alt explanation- dep may= distorted memories, - a third factor eg poverty involved: not loss of affection causing symptoms.
Brown + Harris (1978)- further supp: aim: link between past+current life events + dep. W/C women= more stress M/C males. Proc: interview, LEDS (life events difficulty scale) 539 women, London. their life events rated by researchers how stressful- no know whether dep or not, avoid bias. Looked for associations- dep + recent stress event +childhood.
Findings: recent+childhood high stress= vuln to dep. 80% women w/ dep= stress life event past year: 40% not dep. Eval: -histocentric: mostly based on women. -correlational: just bc bad childhood+ dep doesnt mean caused it: can't infer cause and effect. -methods unscienticic and unfalsifiable.
Conclusion: difficult to disentangle bio and psych reasoning and causality cannot be established, and unclear if changes in biology triggered psychological changes or vice-versa. Likely to be interaction of different factors thus cannot be a single aetiology for depression.
Unipolar Depression- the end <3
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