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A Level Psychology > Depression > Flashcards

Depression Flashcards

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1
Q

Unipolar depression

Biological explanation - Monoamine theory

A
  • The monoamine hypothesis claims that low level of monoamines cause depression.
  • Monoamines consist of noradrenaline/norepinephrine, dopamine and serotonin.
  • Serotonin regulates the other neurotransmitters, so low levels of serotonin leads to lower levels of dopamine.
  • Low levels of serotonin cause erratic brain function and thought patterns.
  • Low levels of noradrenaline cause lower levels of alertness and arousal, symptoms of depression.
  • Low levels of dopamine cause lack of concentration and focus.
  • Low levels of monoamines could be caused because the reuptake mechanism recaptures the neurotransmitters before they reach the receptor sites.
  • Depressed people could release too much monoamine oxidase so the monoamines are broken down too fast.
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2
Q

Unipolar depression

Evidence for biological explanation

A
  • Drevets et al (1999) found reduced serotonin receptor-binding potential in unmedicated depressed patients.
  • Versiani et al (1999) found that patients who had noradrenaline reuptake inhibitors increased their mood if changing the biology can reduce symptoms there may be a biological cause.
  • Bunney et al (1970) found that urinary levels of noradrenaline decreased during episodes of depression.
  • Bell et al (2001) depleted levels of tryptophan and found this caused a relapse of symptoms in depressed patients showing that changing the biology of a person can cause the symptoms of unipolar depression.
  • Delgado (2000) found that monoamine depletion did not make symptoms worse in depressed patients not taking medication.
  • Angoa-Perez (2014) found that mice without the gene for tryptophan did not show signs of depression.
  • Delgado et al (1990) used a special diet to lower the level of tryptophan found that depressive symptoms returned for 67% of ppts.
  • Anti-depressants which increase the monoamines alleviate depression showing reduced monoamines are a possible cause.
  • However, the level of neurotransmitters rises very quickly once an individual is on medication.
  • There are alternative theories such as the cognitive therefore it is not the only explanation.
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3
Q

Unipolar depression

Symptoms

A

Emotional
- Lowered mood and self esteem.
- Anger - negative emotions are more common than positive symptoms.
Motivational
- Activity levels - reduced energy levels which makes them lethargic. This leads to withdrawal from work, education and social life.
Somatic
- Disruption to sleep and eating behaviours
Cognitive
- Poor concentration
- Dwelling on the negative - focus on negative aspects of a situation
- Absolutist thinking - see unfortunate events as a disaster/

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4
Q

Prevalence of depression

A
  • Population - Kesler et al (1994) 10% of adults in the US suffer from severe unipolar depression in any given year, while another 3-5% suffer from mild forms.
    Smith et al found similar stats for Canada, England and other countries.
  • Age of onset - Weismann et al (1992) - average age of onset is 27 in the USE but dropped with each generation from 1915. Severe unipolar depression may develop at any age.
  • Gender - Weismann et al (1991) in most industrialised countries women are twice as likely to suffer from severe episodes of unipolar depression than men. 26% of women may have severe episodes at some point in their life compared with 12% of men.
  • Goldberg (1995) most who do recover are likely to have at least one subsequent episode of depression within lifetime.
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5
Q

Unipolar depression

Evaluation of monoamine hypothesis

A
  • incomplete, describes depression in great depth but not where it comes from. This also applies to cognitive theory which explains depressive thought patterns but only vague ideas why some people develop pessimistic explanatory styles or negative schema’s but others don’t.
  • Twin studies and adoption studies do not show 100% concordance rate. This suggests something non-biological is also a factor, like the environment a person lives in. Genes may give predisposition but require a trigger to bring the symptoms out.
  • Thase et al (2002) found that depresses patients had increased levels of noradrenaline. This is the opposite of what monoamine theory predicts.
  • Twin studies studies show evidence of a genetic aspect to depression. This is because depression is more common in people who are related to depressives than in the general population.
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6
Q

Unipolar depression

Biological treatment - MAOIs

A
  • When released into the synapse serotonin and noradrenaline are broken down by the enzyme monoamine oxidase.
  • This reduces the amount of serotonin and noradrenaline .
  • MAOI’s inhibit the action of monoamine oxidase so results in higher levels or serotonin in the synapse
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7
Q

Unipolar depression

Evaluation of biological treatment - MAOIs

A
  • Seen as being least effective.
  • According to Bennett (2006) they have 50% success rate.
  • Side effects include blood pressure and increased risk or cerebral hemorrhage, especially if taken with yeast products, fish and bananas.
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8
Q

Unipolar depression

Biological treatment - Tricyclics

A
  • Serotonin and noradrenaline are released into the synapse.
  • On the pre-synaptic side where there are re-uptake sites that absorb chemicals.
  • Tricyclics act by blocking these sites so more serotonin and noradrenaline is available in the synapse for a longer period of time
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9
Q

Unipolar depression

Evaluation of biological treatment - Tricyclics

A
  • Have 60-65% success rate.
  • They work on serotonin and noradrenaline pathways, thus have similar side effects. For, example sexual problems, effect the heart and arteries, dry mouth, blurred vision.
  • Potentially lethal in large doses.
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10
Q

Unipolar depression

Biological treatment - SSRI’s

A
  • Inhibit re-uptake, but are selective to serotonin.
  • Treats in the inadequate amount of serotonin in the synaptic gap. This is needed for effective neurotransmitter to occur.
  • SSRI’s work to prevent re-uptake of serotonin, this makes it stay in the synaptic gap longer which makes the serotonin more efficient.
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11
Q

Unipolar depression

Side effects of biological treatment - SSRI’s

A
  • Only alter one pathway, so there is fewer side effects.
  • Almost impossible to overdose on SSRI’s.
  • The most experienced side are dry mouth and constipation however extreme violence and murder have been reported.
  • There have been 250,000 reported cases of suicide, 25,000 of which have been successful. However according to Fergusson et al (2005) there is greater likelihood of suicide with tricyclics.
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12
Q

Unipolar depression

Evaluation of biological treatment - SSRI’s

A
  • All these drugs take weeks to work which suggests their mechanism of action is far more complex than inhibiting re-uptake of serotonin.
  • SSRI’s may work by altering the serotonin system in the brain. Some even believe that there is a change to the natural growth in the hippocampus.
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13
Q

Unipolar depression

Effectiveness of biological treatment - SSRI’s

A

Hollen et al (2005)
- Depressed patients were treated for 16 weeks.
They recieved either: an SSRI or cognitive therapy.
- Similar numbers of each group showed considerable improvement.
Hollen et al (2005)
- Then picked up and followed these successes for 12 months.
- When cognitive therapy therapy was stopped and no further treatment was received, relatively few sufferers relapsed into depression. This suggests that cognitive therapy has dealt with the cause of depression.
- When drug therapy was given and maintained relapse rate is relatively low which suggests the drugs are working.
- 76% relapse when drugs are withdrawn. This confirms that drugs are fine until medication stops. During the prescribed period the drugs reduced symptoms but did not deal with the causes, if they did the patient should be fine when medication was stopped.
- Drugs appear to be palliative.
- Effectiveness dropped from 60% to below 20% in those who had previously been prescribed similar drugs.

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14
Q

Unipolar depression

Cognitive treatment - CBT

A
  • Aims to help people become aware of negative interpretations.
  • Overcome depressive thoughts by changing maladpative interpretations by considering alternative thoughts.
  • Cognitive theory helps people develop alternative ways of thinking and behaving which aims to reduce their psychological distress.
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15
Q

Unipolar depression

Beck cognitive theory- CBT

A
  • 3 mechanisms: cognitive triad, errors in logic and schemata
  • Cognitive triad:
    Consists of negative thoughts
    Unpleasant experiences are attributed to personal worthlessness.
    Depressive, negative thoughts about experience consist in the interpretation that when somethings happens, it is perceived to be bad.
  • Genetic factors and early experiences affect thinking and schemata are built from interactions and experiences, involves developing positive and negative beliefs to interpret the world.
  • A generalised negative belief will make someone vulnerable to depression.
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16
Q

Unipolar depression

Seligman (1967) - CBT

A
  • Depression is a form of learned helplessness, which is when people have learned to give up trying to put things right because they only experienced failure.
  • Use of dogs showed how a concept they called learned helplessness can cause a pessimistic victim pf abuse to fail to identify and use escape routes.
  • A dog is into a partitioned cage, learns to escape when floor is electrified.
    If dog is restrained whilst being shocking it eventually stops trying to escape.
  • Dogs restricted to this later failed to escape when it was possible to escape.
  • This lead to Seligman to explain depression in humans in terms of learned helplessness, where the individual gives up trying to influence their environment because they have learned that they are helpless as consequence of having no control over what happens to them.
17
Q

Unipolar depression

Research evidence of cognitive treatment - CBT

A

Alloy and Abramson (1999)
- Longitudinal study of those with depression to evaluate Becks theory. Identified college students who had negative self-schemata.
- Researchers found that students with negative though patterns were more at risk from depression.
Watkins and Barcaia (2002)
- Found that knowing about mental process helped to reduced relapse in those with depression and helped to stop them continually going over problems in their head.
Bothwell and Scott (1997)
- Found that faulty thinking and errors in cognitive processing. Especially with regard to needing approval and low self-esteem linked with symptoms of depression continuing after hospital care.

18
Q

Unipolar depression

Limitations of cognitive treatment - CBT

A
  • Ellis’s highly confrontational method may be too much for some emotionally fragile patients
  • Embling (2002) CBT tends not to work well for highly perfectionists and patients with a high external locus of control.
19
Q

Unipolar depression

Cultural differences

A
  • Cross-cultural study by Bromet et al (2011) sampled 70,000 people in 18 countries. France and USA were the most depressed and the poorer countries showed less rather than more depression. This supports the idea that depression is a disorder of Westerns nations, not just a psychological response to poverty, crime or war.
  • Gert Hofstede claims that individualistic cultures are more prone to depression but collectivist cultures offer more support. This is supported by a cross-cultural study by Chiao et al (2009). Suggests that people in Eastern countries have a greater genetic susceptibility to depression but have developed a collectivist culture as a way of reducing it; Westerners are less susceptible and have developed an individualistic culture although leaves them more at risk. This is using evolutionary psychology to explain culture and mental health.
20
Q

Unipolar depression

Developmental differences

A
  • Children of the 90s is a longitudinal study by the University of Bristol, which recruited 14,000 pregnant woman in the early 1990s and follows their children and families. A recent analysis by Culpon et al (2013) of 5631 whose fathers left home when they were between 0 and 5 shows they are more at risk of depression than those whose fathers left when they were older.
  • People are most likely to experience their first depressive episode between 30-40 and there is a second, smaller peak of onset between 50-60.
21
Q

Unipolar depression

Gender differences

A
  • Population studies have consistently shown clinical depression to be twice as common in women as men (Beddington, 1996) although it is unclear why this is so.
  • Social explanation: women experience greater social isolation, poverty and domestic abuse.
  • Cognitive explanation: women experience more stress and confusion over life choices (whether to pursue a career or to raise children) and anxiety in society (fear of crime and sexism)
  • Biological explanations; women’s brains seem to have more serotonin receptors than male brains and serotonin is biological explanation for depression.
22
Q

Unipolar depression

Personality differences

A
  • High N and low E are linked with depression. However this describes depression and does not explain it. Depressed people experience anxiety and they withdraw from social relationships.
    Brown et al (1985)
  • Identify self-esteem as an impairment in personality trait that acts as protection against the onset of depression during stressful life events. However they also identify situational variables that are just as important for protecting against depression, such as social impact.

A Level Psychology (4 decks)

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