The Psychology of Depression

*Classified under the DSM-IV-TR as a mood disorder.
Major Depressive Disorder.

• Affective symptoms = depressed mood, sadness, feeling low.
• Cognitive symptoms = feeling guilty, thinking they are worthless.
• Behavioural symptoms = social withdrawal, restlessness.
• Physical symptoms = changes in sleep patterns, energy levels or appetite.

Requires the presence of five of the following:

• Sad, depressed mood.
• Loss of interest and pleasure in usual activities.
• Difficulties in sleeping.
• Shifts in activity level, lethargic or agitated.
• Poor appetite and weight loss, or increased appetite and weight loss.
• Loss of energy and great fatigue.
• Negative self concept, feelings of worthlessness and guilt.
• Difficulty in concentrating.
• Recurrent thoughts of death or suicide.
  

*Keller et al: suggest that inter-rater reliability (DSM classification) is 'fair to good'.
suggest that test-retest reliability (DSM classification) is just 'fair' at best.
*Similar conclusion reached by Zanarini.

*Keller: suggests a number of reasons why it lacks reliability.
a) a minimum of 5 out of 9 symptoms must be present.
b) a one-item disagreement can make the difference between MDD and a less serious illness.

*McClough et al: found considerable overlap in symptoms, responses to treatment and othe variables (when comparing various types of depression).
= difficult to justify different forms of the illness.

*GP diagnoses:
- may be less objective because they are based on previous knowledge rather than the symptoms. [N.B this could be argued to be both an disadvantage/advantage].

Limitations of the DSM.

*gender and culture bias as made by western males.

*difference in normative values between western and non-western societies.

*ignores individual differences?

*may be another cause for behaviour.

*An individual's normative behaviour, personality and history are different.

*subjectivity - GPs.

*degree of symptoms - how far is this taken into account?

*depression is stigmatised in some cultures.

Genetic factors

• Having a first degree relative with depression seems to be a risk factor for depression.
• Probands' relatives have showed higher rates of depression (20%) than in the general population (10%).
• McGuffin: concordance rate was 46% for identical twins and 20% for fraternal twins.
• Wender: higher incidence of severe depression in biological relatives of the depressed group, than the biological relatives of a non-depressed control group.
• Genes as a diathesis - genetic predisposition.
• Kendler: women who were a co-twin of a depressed sibling were more likely to become depressed than those without this genetic vulnerability.
• Kendler: highest levels of depression for those exposed to negative life events and genetically at risk.

Limitations/Research Support

*a mutant gene that starves the brain of serotonin 10 times more prevalent in depressed.
= Caron: version of the gene was carried by 9 out of 87 depressed patients, but only of 219 controls, and patients with the mutation failed to respond well to SSRIs.

*low genetic concordance rates may be explained by comorbidity.

*maybe people inherit a vunerability for a wider range of illnesses.
= Kendler: higher incidence rate for twins when looking at depression and general anxiety disorder than when looking at depression alone.

*diathesis-stress model.

*nature vs. nurture.

*deterministic, reductionist.

Amine Hypothesis

Low activity of monoamine transmitters (noradrenaline, serotonin) will result in depression.

Act as chemical messengers in the brain, affecting parts concerned with reward/punishment.

Some are involved in the regulation of the hypothalamus - affects appetite, physical movement, sleep, sexuality.

If there is low activity in the monoamine transmitters then some of these areas will be affected and create symptoms of depression. (e.g loss of appetite).

In-direct markers of noradrenaline were often low in depressed (e.g. by-products found in urine).

Antidepressants confirm the association between low serotonin and depression.

Limitations/Research for Neurotransmitter dysfunction/Amine Hypothesis
*Leonard: drugs that lower noradrenaline bring about depressive states, while those that increase levels show antidepressant effects.

*Kraft: treated patients with a SNRI (dual serotonin-noradrenaline re-uptake inhibitor) - showed more positive response than those treated with a placebo.

*Antidepressants increase the activity of monoamines - effective in alleviating depressive symptoms.
- BUT, have more than one affect on the brain.
- unclear whether it is exactly the low activity of monoamines that creates depressive symptoms.
- Immediate effect on neurotransmitter levels, several weeks to have an effect on the symptoms of depression?

*Cause or consequence?

*Deterministic, reductionist.

Psychodynamic Approach.

Mourning and Melancholia - mourning period when loved one lost.
For some, this period never ends = exist in a state of permanent melancholia.
Mourning is a natural process, melancholia is a pathological illness.

'Anger turned against oneself' -unconsciously harbour negative feelings towards loved one.
These feelings are turned upon ourselves when we lose them.
Might resent being deserted.
This period, followed by a period of mourning (recall memories etc).
Process may go astray = continue a pattern of self abuse and self blame.
So depression is 'anger turned against oneself'..

Limitations/Research.

Barnes and Prosen: men who had lost their fathers through death during childhood scored higher on a depression scale than those whose father's had not died.

Bifulco: children whose mothers died in childhood were more likely than others to experience depression later in life.
- BUT could be explained by lack of care from parents and parent substitutes following the loss, rather than the loss itself.

Loss probably only explains a small %. Approx. 10% of those who experience early loss develop depression..

Psychoanalysis has not proved effective with cases of depression.
- BUT, this may be because depressed people may find it difficult to communicate in the way required.

Cognitive.

Beck's Theory of Depression.

• Thinking is biased towards negative interpretations of the world.
• Acquired a negative schema during childhood.
• May be caused by some kind of rejection.
• Neg. schema activated when encounter a new situation which resembles the original.
• Neg. schema subject to cognitive biases in thinking.
• Neg. schema and cog. biases maintain the negative triad.
• A pessimistic view of the self, the world and the future.

Cognitive: Beck's Theory of Depression.

Limitations/Research.

Bates: depressed patients who were given negative automatic thought statements became more and more depressed.

Hammen and Krantz: depressed women made more errors in logic when asked to interpret written material than non-depressed.

However, though there is a link between negative thoughts and depression - doesn't mean it is the cause. Could be a consequence!

Associated with successful therapies.

Less deterministic than biological approach.

Doesn't take into account biological factors. Nature vs. Nurture.

Cognitive: Learned Helplessness.

A person tries but fails to control unpleasant experiences.
Acquire a sense of being unable to exercise control over their life.
So become depressed.

This learned helplessness then impairs performance in situations that can be controlled.

Seligman: depressed people thought about unpleasant events in more pessimistic ways than non-depressed.

The 'reformed helplessness theory': depressed person thinks the cause of such events is internal, stable and global.

Depressive attributional style = attribute outcomes to personal, stable and global character faults.

Cognitive: Learned Helplessness.

Limitations/Research.

*Seligman's initial research on animals - implications? ethics?

*Seligman and Hiroto: showed that college students who were exposed to uncontrollable aversive events were more likely to fail on cognitive tasks.

*Seligman and Miller: depressed students performed worst on a similar task.

*Findings show that having some degree of control improves performance.

*Cognitive explanations have successful therapies.

*Nature vs. Nurture.

Antidepressants.

• Work by reducing the rate of re-absorption or by blocking the enzyme which breaks down neurotransmitters.
• These increase the amount of neurotransmitters available to excite neighbouring cells.
• Tricyclics block the transporter mechanism that re-absorbs both serotonin and noradrenaline.
• SSRIs (Selective Serotonin re-uptake inhibitors) block the re-uptake of serotonin.
• Three phases of treatment: Acute, Continuation and Maintenance.
• Acute = treatment of current symptoms.
• Continuation = medication is gradually withdrawn to prevent relapse.
• Maintenance = recommended for individuals who have a history of recurrent depressive episodes.

Antidepressants: Limitations/Research.

• Kirsch: clinical trials of SSRI antidepressants - only in severe cases was there any advantage in using SSRIs.
• In only the most depressed patients was there a difference between drugs and placebos.
• Indicates that placebos 'offered them hope'.
• Presumably the expectation for anything working was lessened in the most depressed, diminishing the placebo effect.
• May be publication bias - tend to publish studies which show a positive outcome of antidepressant drugs.
• less useful for children - developmental differences in brain.
• SSRIs/other treatment/placebo = those treated with SSRIs twice as likely to attempt suicide.
• However, found that SSRIs increased risk in adolescents, but decreased it in adults.

Electroconvulsive Therapy (ECT).

Injected with an anesthetic and a nerve-blocking agent.
A small amount of electric current is passed through the brain, lasting for about half a second. This produces a seizure lasting up to one minute, which affects the brain.

Generally given 3 times a week with the patient requiring between 3 and 15 treatments.

How or why it works it not understood. BUT it is the SEIZURE not the electrical stimulus which causes the change. It appears to restore the brain's ability to regulate the mood.

• Unilateral = electrode placed above the temple of the non-dominant side of the brain and the second, in the middle of the forehead.

• Bilateral = one electrode placed above each temple.

ECT: Limitations/Research.
*ECT vs. 'sham' ECT = found a significant difference in favour of the real ECT.

*Effective in cases of treatment-resistant depression, although there have been studies which show no difference.

*18 studies with 1144 patients comparing ECT with drug therapy - ECT is more effective in short term treatment.
*None of these studies compared ECT to newer antidepressants such as SSRIs.

*Possible side effects = impaired memory, cardiovascular changes, headaches.

*At least 1/3 of people complained of persistent memory loss.
& 30% have reported that it had resulted in permanent fear and anxiety - over 2 years worth of patients.

*unilateral ECT is less likely to cause cog. problems than bilateral.

*Informed consent? Deception?

Cognitive-Behavioural Therapy (CBT).

• Emphasises the role of maladaptive thoughts and beliefs in the origins and maintenance of depression.
• Identify and alter these cognitions, and any dysfunctional behaviours.
• Intended to be relatively brief.
• Focus is on current problems and feelings.
• 'Thought Catching' and 'Behavioural Activation'.

Thought Catching = link between thoughts and the way they feel, could record:

• emotion arousing events.
• the automatic 'negative' thoughts associated.
• their 'realistic' thoughts that might challenge negative ones.
• replace dysfunctional thoughts with constructive ones.

Behavioural Activation = being active leads to rewards = antidote to depression.

• identify potentially pleasurable activites.
• anticipate and deal with any obstacles.

Limitations/Research of CBT.

*Meta-analysis: CBT superior to no-treatment controls. BUT, when controls divided into waiting list and placebo - CBT not significantly more effective than placebo.

*Therapist competence: explain variation of CBT outcomes - as much as 15% of the variance in outcome may be attributed to this.

*Client's engagement with homework predicts outcome.

*Successfully applied to many different groups e.g. elderly, juveniles and adolescents.

*Can be computer-based - which has a low drop out rate.

*Less suitable for people with high dysfunctional beliefs, or where high levels of stress in the individual reflect realistic stressors in life that therapy cannot resolve.

Psychodynamic interpersonal therapy (PIT).

• attempt to move away from traditional psychoanalytic approach of a one-sided relationship between client and therapist.

• 'conversational model' = mutual task to engage in therapeutic 'conversation'.

• problems are not only talked about as past events, but are actively relived in the present and resolved within the relationship.

• believed that symptoms of depression arise from disturbances in interpersonal relationships.

• these disturbances can only be explored and modified effectively from within another relationship - the therapeutic one.

Limitations/Research of PIT.

*PIT has been shown to be at least as effective as CBT. However, in these studies life events were not monitored during the study, therefore any observed gains (or lack of) could not be attributed solely to the therapeutic intervention.

*Collaborative Psychotherapy Project: PIT and CBT were equally effective in reducing the severity of depression. However, after 12 months, those treated with PIT or CBT showed a tendency for symptoms to recur - limiting long-term effectiveness.

*quality of the relationship between therapist and client is a central determinant of the outcomes of therapy.

*12 weeks of PIT by psychiatry trainees/ waiting list = significant improvement was observed in patients who completed therapy - suggests that even brief therapy by inexperienced trainees can be effective.