Depression Flashcards
Affective symptoms
Mood
Bodily symptoms
Physical
- changes in weight and appetite
- aches and pains
- low sex drive
- lack of energy / disturbed sleep
Cognitive symptoms
Psychological
- sadness
- low self esteem
- feeling anxious and worried
- suicidal thoughts
Behavioural symptoms
Social
- neglecting hobbies
- avoiding contact with friends
- taking part in fewer social acitivities
Features of depression
- more common in women than men
- co-morbid with many other physical and mental disorders e.g. anxiety / 23% of women with ovarian cancer have depression
- anhedonia = lack of enjoyment found in previously enjoyed activities events and places
- first year of covid = depression and anxiety increased by 25%
Issues with the diagnosis of depression
- many cultures don’t recognise depression an doesn’t have a word in their langauge which fully holds the same English connotations
- in different cultures, depression is manifested through different symptoms
- Regier et al (2013) = field trials of DSM-5 used kappa stats to measure agreement between diagnostic practitioners (value of 0.28) for depression so very questionable reliability
Strengths with the diagnosis of depression
- structured clinical interview for DSM-5 (SCID-5) is usually used for real world diagnosis
- DSM-5 includes how to conduct a cultural formulation interview (how one’s cultural identity may affect expressions of signs and symptoms)
Biological explanation - monoamine depletion hypothesis
- group of neurotransmitters (includes serotonin dopamine and noradrenline) that regulate mood and function of the limbic system
- permissive hypothesis = interaction between serotonin and noradrenaline is the cause of depression rather than serotonin alone. Low levels of serotonin permits noradrenaline to decrease as well
- low serotonin is necessary for depression but not sufficient on its own
Monoamines
A group of neurotransmitters that regulate mood. Includes serotonin, dopamine, noradrenaline
Biological explanation - receptor sensitivity hypothesis
- low levels of serotonin so post synaptic receptors increase sensitivity to gather as much serotonin as possible (upregualrion)
- take an antidepressant
- higher levels of serotonin but super sensitive post synaptic receptors are now overstimulated
- post synaptic receptors decreases sensitivity due to too much serotonin (downregularion)
- after 4 to 5 weeks, sensitivity will come to an equilibrium
BDNF
Brain Derived Neurotrophic Factor = a chemical which feeds neurons the nutrients they need to survive, grow and function efficiently. Plays a key role in neuronal plasticity (ability to form new synapses
BDNF hypothesis
- levels of BDNF are abnormally low in the hippocampus and prefrontal cortex of depressed patients (lower the levels, the more severe the symptoms)
- links depression with stress as the gene for BDNF switches off under stress, leaving the neurons fed by BDNF vulnerable to atrophy (cell shrinkage) or apoptosis (cell death)
Bio explanation AO3- therapeutic delay
- monoamine hypothesis can’t explain therapeutic delay as it takes 4-6weeks for antidepressants to find improvement in symptoms
- however receptor sensitivity hypothesis explains this due to up and downregulation which is not immediate (several weeks) so correlates either symptom improvement
Bio explanation AO3 - Sen et al (2008)
negative correlation between blood serum levels of BDNF (abnormally low) and the severity of depressive symptoms
(HOWEVER, correlational not causational)
Bio explanation AO3- Matrinowich et al (2007)
Post mortem study. Abnormally low levels of BDNF in the hippocampus and prefrontal cortex in people who had depression
(HOWEVER, correlational not causational)
Bio explanation AO3 - Treatment aetiology fallacy
- The treatment is biological but the cause is psychological
- postsynaptic receptors were downregulation by antidepressants that increased serotonin so researchers believe if biochem treatment improves symptoms, depression must have a biochem cause. HOWEVER not necessarily true - antidepressants work by correcting a biological process that is triggered by a psychological factor e.g. stress
Bio explanation AO3- Application
- recent drug treatments target both serotonin and noradrenline levels (duloxetine) as opposed to serotonin only (supports monoamine hypothesis)
- BDNF offers a different type of biological treatment (TMS)
- treatments may improved quality of life and reduce stress
Bio explanation AO3 - Man (2003)
Post mortem studies for suicide = low serotonin and high number of serotonin sites
Cognitive explanation of depression - Beck (1967)
faulty or irrational thinking is a symptom of depression that may also be the root cause
Beck (1967)- negative cognitive triad
Faulty cognitions stem from childhood via criticism and rejection by parents and teachers as well as expressive and unrealistic expectations and experiences of loss which creates pessimism
Beck (1967) - depressed people make 3 major types or cognitive errors…
1) the self = believes they are worthless, a failure, unattractive etc which confirms their feelings of low self esteem
2) the future = the future is unavoidably negative, bleak, nothing to look forward to
3) the world = the world is hopeless e.g. if friend cancels, one believes no one likes them
Cognitive explanation - Ellis (1952) ABC theory
Focused on irrational thinking and how this causes depression. Anything other than thinking that allows us to be happy and free from psychological pain is irrational
Ellis (1962) - Activating event
Irrational thoughts are triggered by the situation. Negative external events activate irrational thoughts
Ellis (1962) - beliefs
Persons beliefs about the event cause depression, not event itself. Types of irrational beliefs:
- musterbation= “I must be perfect, successful and attractive”
- Utopianism = the belief that life should always be fair
- I can’t stand it itis = something is not going perfectly amounts to a major disaster
Ellis (1962) - consequences
Irrational beliefs have emotional and behavioural consequences
E.g. one who believes “life is fair” becomes depressed when it’s not/ “I must be successful” could react bad,T to failure
Cog explanation AO3 - Evan’s et al (2005)
- measured self believes of 12003 women at 18 weeks pregnant
- those with most negative beliefs were more likely to become depressed even after 3 years
- negative cognitions occurred before depression
- aetiological validity
Cog explanation AO3 - Eysenck (1997)
- No independent way of establishing the existence of negative schemas
- doesn’t explain depression or identify risk factors and cannot predict who is likely to become depressed
- lacks predictive validity
- becks theory suggest how it is triggered and maintained not how it is caused
Cog explanation AO3 - Application
- challenging irrational beliefs of depressed person came improve symptoms
- led to Becks Cognitive Behavioural Treatment (CBT) - therapist encourages client to test whether negative triad is true
- cognitive techniques are part of successful treatments so implies faulty information processing is the root of disorder
Cog Explantion AO3 - weaknesses
- neither theories can fully explain all aspects of depression
- depression is complex - not everyone experiences it the same way so hard to see how negative cognitive triad and dysfunctional beliefs account for a variety of experiences - incomplete explanation
- evidence that negative thinking accompanies depressio, little that is causes it
- negative self beliefs is only a symptom of depression, not a causation as beliefs usually become positive one depressive episode is over
Bio treatment - monoamine-oxidase inhibitors (MAOIs)
- after neurotransmission, serotonin molecules are reabsorbed by the presynaptic cell (uptake)
- they are broken down into chemical constituents by the enzyme monoamine oxidase (MAO)
- MAOIs block the MAO to increase the availability of serotonin for future realise into the synapse
- MAOIs increase all monoamine neurotransmitters (serotonin, dopamine, noradrenaline etc)
E.g. tranylcypromine
Bio treatment - selective serotonin Reuptake inhibitors (SSRIs)
E.g. Prozac, paxil
- serotonin in the synapse is normally Reuptaken into presynaptic neuron via the serotonin transporter
- SSRIs block serotonin transporter so serotonin can’t be recycled and remains in synapse for further use
- this prolongs antidepressant effects of serotonin through repeated binding with receptors on postsynaptic neuron
Bio treatment - Sertonin-noradrenaline reuptake inhibitors (SNRIs)
E.g. duloxetine
- works in a similar way to SSRIs but targets noradrenaline as well as serotonin
- inhibits reuptake of both neurotransmitters
Bio Treatment - noradrenergic and specific serotonergic antidepressants (NaSSAs)
E.g. mirtazapine
- used for those who haven’t benefited from SSRIS ANS SNRIS due to bad side effects/ineffectiveness
- inhibits reuptake of serotonin and noradrenaline but to a much lesser extent
- NaSSAs are antagonists of serotonin and noradrenaline receptors (block them)
- NaSSAs block serotonin receptors 5-HT2 and 5-HT3 which increases activity of the key 5-HT1A receptor
Bio treatment AO3 - Cipriani et al (2018)
- meta analysis
- studies of 22 antidepressants, 552 double blind trails involving over 116000 randomly allocated pps
- all drugs more effective than placebo as drugs improved mood of depressed
HOWEVER… - most effective drugs = worst compliance rates (ppl stopped taking them) = unreliable
- side effects were “mostly modest” = individual differences so not all drugs are equally useful to different people so unreliable
Bio treatment AO3 - Kirsch et al (2008)
- reviewed 47 trials of patients with mild or severe depression prescribed SSRIs or placebo
- patients w severe depression had a greater response to antidepressants than placebos
HOWEVER… - SSRIs aren’t better than placebo with mild depression
- 1 in 4, drug treatments made patients worse due to side effects
Bio treatment AO3 - weaknesses
- drug treatments relieve symptoms but don’t tackle the causes - genetic or environmental cause will remain
- only 70% of patients benefit from drug treatments
- Recovery Movement = the idea that medical drug companies push medication onto ppl to boost profits
Bio treatments AO3 - strengths
- it’s a common belief that depression is a psychological weakness due to laziness and mindset but drugs explain it’s a medical disorder so removes stigma therefore encourages ppl to seek treatment which is has ethical applications
- knowing about side effects of drugs helps one to manage them which improves acceptability and credibility
Non bio treatment - Becks Cognitive Behavioural Treatment (CBT) assessment
Whole procedure usually 20 session over 16 weeks
- therapist and client assess various aspects of clients functioning
- therapist uses interviews and questionnaires to measure depression and any comorbid disorders
- both identify specific issues, list goals and construct a plan
- key task = identify clients negative thoughts and re-evaluate them to avoid relapse
Non bio treatment - CBT - role of education
- client has active role of implementing therapy plan to understand nature to their symptoms
- therapist explains techniques to help
- together they decide what is most helpful and what should be carried out
- therapist viewed as a helper of clients self discovery
Non bio treatment - CBT - role of homework
- client needs to carry out plan in real life
- Homework = chance to test reality of negative thoughts and get evidence for and against them
E.g. client writes down when someone was nice to them at an event so when later they say “everyone hates me” therapist will show evidence to prove it’s not true
Non bio treatment - Ellis REBT
- therapist challenges irrational thoughts through dispute
- replace them with reasonable ones
- more about persuasion and confrontation as REBT views therapist as a teacher
Non bio treatment - REBT - two forms of dispute
1) logical dispute = therapist questions the logic of irrational thoughts through
E.g. “why would your friend not want you to go to the cinema with them?”
2) empirical dispute = therapist asks for evidence for irrational thoughts
E.g. “what evidence do you have to prove that they don’t want to see you?”
Non bio treatment AO3 - Elkin et al (1989)
- randomly allocated pps to 1/4 treatment groups
- CBT around just as effective at reducing symptoms as medication so valid therapy
HOWEVER… - CBT not as useful in severely depressed patients as antidepressants were significantly more effective
Non bio treatment AO3 - DeRubeis et al (2005)
CBT can be equals effective for mild, moderate and severe depression
Non bio treatment AO3 - Easterbrook and Mechan (2017)
- case study of depressed adolescent female
- collaborative relationship with therapist established open communication before techniques
- effectiveness of CBT is due to quality of therapeutic relationship
Non bio treatments AO3- strengths
- gives patient control over disorder and power to change
- allows opportunity to use homework strategies in a range of similar situation
- can be very successful and long lasting
- no real side effects or withdrawal symptoms
Non bio treatments AO3 - weaknesses
- doesn’t always deal with root cause
- effectiveness depends on severity
- not suitable for people with rigid attitudes
- can take months to see improvement unlike drugs
- doesn’t focus on why negative beliefs are held
- negative beliefs may just be suppressed rather than eliminated leading to relapse
- is expensive and time consuming
