Depression

• Monoamine depletion hypothesis (Schildkraut 1965) states: depletion of monoamines in the brain leads to depression
• Latest version of the monoamine hypothesis

  depression = caused by imbalance of seratonin and noradrenaline

  • abnormally low seratonin = decreased noradrenaline aswell
  • low seratonin is necessary for depression but not enough on its own
• Receptor sensitivity hypothesis states: there is more to depression than monoamine depletion, and that depression is caused by changes in the sensitivity of postsynaptic receptors
• Normal response of receptors to NT depletion = upregulation (increase no. of receptors = more sensitive to NTs)
• BDNF hypothesis: low BDNF in hippocampus and PFC = depression.

  There is an inversely proportional relationship between BDNF levels and symptom severity.
• Credibility for bio explanation of depression:

  Sen et al. (2008) - negative correlation between blood serum BDNF and the severity of depressive symptoms; post-mortems of depressed people have found abnormally low BDNF in the hippocampus and PFC. This study along with Martinowich et al. (2007), both show a clear association between BDNF level and depressive symptoms.
• BDNF hypothesis links depression with stress...

  • gene for BDNF may be switched off under stress
  • neurons fed by BDNF are vulnerable to atrophy and apoptosis
• Objections for bio explanation:

  • monoamine hypothesis was seen as being reductionist (cannot explain therapeutic delay and why levels of seratonin and noradrenaline increase immediately and within a week, are normal)
• Differences for bio explanation: (1)

  receptor sensitivity explains therapeutic delay = antidepressants increase the availability of serotonin and/or noradrenaline in the synapse, as a result there is a corresponding downregulation in postsynaptic receptors to compensate for the greater stimulation.
• Differences for bio explanation: (2)

  Treatment aetiology fallacy = people assumed that if a biochemical treatment improved the symptoms of depression then depression must have a biochemical cause: this isn’t true as a drug could work by correcting a biological process that is disturbed by a psychological factor (stress).
• Applications for bio explanation:

  Better understanding of neurochemistry: recent drug treatments target both seratonin and noradrenaline levels (ie duloxetine). GABA and dopamine are attracting interest as targets for medication, and BDNF offers yet another route involving a different type of bio treatment.
• MAOI's weaken the reabsorption of the NT's chemical components by inhibiting the activity of the enzyme monoamine oxidase. Serotonin must remain in the synapse for further use because it escapes degradation. Hence, MAOI's raise levels of dopamine and noradrenaline.
• SSRIs block the serotonin transporter, so serotonin cannot be recycled and remains in the synapse for longer. This prolongs the antidepressant effects of serotonin through repeated binding with receptors on the postsynaptic neuron.
• SSRIs may take up to 4 weeks before the full effect is felt.
• SNRIs are a newer gen of antidepressants that were developed to reflect the understanding that noradrenaline plays a key role in regulation of mood.
• SNRIs work in a similar way to SSRIs, but target noradrenaline as well as serotonin, inhibiting the reuptake of both NTs.
• NASSAs are useful if SSRIs and SNRIs are not working well, and they:

  • inhibit reuptake of serotonin and noraadrenaline (but much less than SSRIs and SNRIs)
  • are antagonists of serotonin and noradrenaline receptors
• NASSAs block 5-HT2 and 5-HT3 and then increase activity of 5-HT14 and also block a noradrenaline receptor.
• Credibility for bio treatment:

  • Cipriani et al (2018): reviewed published+unpublished studies of 21 antidepressants in 522 double-blind trials involving around 116,000 depressed people and drugs were found to be more effective = ambitious demonstration showing that antidepressants can improve mood
• Objections for bio treatment:

  • Cipriani 2018 also found that some of the most effective drugs were also the ones with the worst compliance rates = any antidepressant will lift mood but factors such as individual differences mean antidepressants are not universally useful
• Differences for bio treatment:

  • drugs only relieve symptoms, not tackle the cause = effective antidepressants only stabilise the dysfunctional serotonin circuits in the brain for as long as the person takes the drug. Symptoms such as low mood improve but the genetic cause of depression still remains. The benefit of drugs are limited in the long-term.
• Applications for bio treatment:

  • knowing about side effects helps to manage them = most side effects are common and mild but some may be rare and severe (ie MAOIs interact with other drugs and with chemicals in food). These issues can be controlled with careful monitoring of the persons diet and additional medication = ability to manage side effects, increases the credibility and acceptability of the treatment so people are likely to continue with it
• Beck's cognitive model of depression (1967) focused on faulty/irrational thinking being a symptom of depression AND the root cause.
• The negative cognitive triad stems from childhood via criticism from parents/teachers as well as distorted expectations. Beck argued that depressed people make 3 major types of cognitive error.
• • The self: person believes they are worthless, a failure etc. (low self-esteem)
  • The future: person views the future in avoidable negative ways (bleak and offers nothing of value)
  • The world: person perceives the world around them as hopeless
• Ellis' ABC theory (1962):

  • Activating event = irrational thoughts are not automatic but triggered by the situation
  • Beliefs = it is the person’s beliefs about the event that causes depression, not the event itself
  • Consequences = irrational beliefs have emotional and behavioural consequences
• Cognitive errors:

  • magnification (problems exaggerated)
  • minimisation (strengths+weaknesses are under-emphasised)
  • personalisation (client blames themselves for thigns that are not in their control)
  • polarised thinking (everything is seen as black+white with no in between)
• Credibility for psych explanation:

  Evans et al. (2005) measured self-beliefs of 12,003 women who were 18 weeks pregnant. Those with the most negative beliefs were more likely to eventually become depressed than those with +ve beliefs = these cognitions occurred before the onset of depression, supporting Beck’s view that negative beliefs cause depression
• Objections for psych explanation:

  Dohr et al. (1989) found that negative self beliefs expressed during a depressive episode usually become positive afterwards.

  Brown (2007) states that yes negative thinking accompanies depression, but there isn't enough evidence suggesting that it CAUSES depression.
• Differences for psych explanation:

  • neither Beck’s nor Ellis’ theories can explain all aspects of depression as it is a complex disorder with many features. Not everyone experiences all of the symptoms and there are individual differences in severity; which makes it hard to see how the cognitive triad and dysfunctional beliefs can account for the variety of experiences of depression
• Applications for psych explanation:

  Both theories led to effective treatments for depression = Lipsky et al (1980) support Ellis’ view that challenging irrational beliefs can improve symptoms + Beck’s CBT identifies the components of the negative triad with the therapist encouraging the client to test whether they are true = cognitive techniques successfully treat depression, implying faulty info processing may be at the root of the disorder
• CBT was developed from Beck’s cognitive model of depression. Depression can be treated by helping the individual focus on their negative automatic thoughts (NAT’s) and consider new ways of thinking.
• Assessment

  • process starts with a quick assessment of the clients current functioning
  • may be done via a questionnaire/interview to measure depression and any co-morbid disorders
  • therapist and client identify specific issues, list the goals for therapy and construct a plan
• Role of Education

  • clients need to clearly understand the nature of their symptoms as they have an active role in implementing the therapy plan
  • as therapy progresses, techniques are suggested + explained
  • together they decide what is most helpful + how it should be carried out
• Role of Homework

  • client needs to carry out the plan irl, hence homework gives them a chance to test the (un)reality of their -ve beliefs
  • if the client writes down the details of something they enjoyed, then later on contradict that thought, the therapist can encourage them using their own notes to prove that their negative beliefs are wrong
• A typical session

  Dobson (2008) described a typical session:

  1. quick assessment of clients current functioning
  2. homework is then discussed - why it wasn't completed/what was learnt from it
  3. client chooses most important issues to discuss
  4. if agenda item is a good opportunity to introd. CBT = therapist may use 3-Q technique to challenge the clients ANT's
  5. 3 Q’s = ‘’What’s the evidence? What are the alternatives? So what?’’
  6. clients address cognitive distortions
  7. can explore possibility that ANTs may not be the only interpretations of an event
• Credibility for psych treatment:

  • Elkin et al (1989) randomly allocated 239 participants diagnosed with depression to one of 4 treatment. CBT was as effective in reducing symptoms as interpersonal therapy, antidepressants, or a placebo pill + effectiveness continued after 18 months = CBT is a successful treatment for mild to moderate depression in the short + longer term
• Objections for psych treatment:

  • however CBT was not effective in preventing relapse - after 18 months, 36% of CBT clients relapsed, at a higher rate than in the interpersonal therapy group
• Differences for psych treatment:

  • CBT concerns therapeutic relationship - Easterbrook and Meehan (2017) concluded that a collaborative relationship being established before using CBT encouraged more open communication = practitioners might improve outcomes if they focus on clinician-patient rapport
  • treatment adherence is an issue - CBT is hard for those who may not benefit w/o the help of an antidepressant as it requires dedication and commitment = high dropout rates which are costly for the NHS
• Applications for psych treatment:

  • CBT can help prevent relapses - unlike bio treatments, CBT teaches skills and techniques they apply for themselves which does not require a therapist in the future as the use of homework allows independence whilst respecting the autonomy and dignity of the client
  • CBT uses downward arrow technique = uses the problem to work down to find the cause