The behavioural, emotional and cognitive characteristics of depression.
What is Depression?
Unipolar vs Bipolar Depression
Unipolar depression is characterised as someone experiencing frequent episodes of depressed mood, whereas an individual with Bipolar depression will swing between episodes of depression mood and ‘mania’. Mania is defined as periods of excitement, euphoria and overactivity. The image below highlights the main differences between unipolar and bipolar depression.
Depression is twice as common in women than in men, however men are more likely to commit suicide. Another type of depression is postpartum depression, otherwise known as postnatal depression, which occurs almost exclusively in women.
DSM-5 Criteria for Major Depressive Disorder
Below is the clinical criteria for MDD, as seen in the DSM (used in America). There are four main types of symptom:
• Depressed mood or a loss of interest or pleasure in daily activities for more than two weeks.
• Mood represents a change from the person’s baseline.
• Impaired function: social, occupational, educational.
• Specific symptoms, at least 5 of these 9, present nearly every day:
A1. Markedly diminished interest or pleasure in all or almost all activities most of the day nearly every day.
2. Significant weight loss when not dieting or weight gain.
3. Inability to sleep or oversleeping nearly every day.
4. Psychomotor agitation or retardation nearly every day.
5. Fatigue or loss of energy nearly every day.
6. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day.
7. Diminished ability to think or concentrate, or indecisiveness, nearly every day.
8. Recurrent thoughts of death, suicide, or a suicide attempt or has suicide plan
B. Symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning
C. The episode is not due to the effects of a substance or to a medical condition
D. The occurrence is not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other psychotic disorders
E. There has never been a manic episode or a hypomanic episode
Studies have indicated that there may be a genetic link for depression. McGuffin (1996) studied 214 pairs of twins, where at least one of each twin pair was being treated for unipolar depression. It was found that 46% of the identical twins shared the disorder, and only 20% of fraternal non-identical twins shared the disorder. This indicates a genetic link, since DZ twins only share 50% genetics, yet are likely to also share the same environment.
This research support Allen (1976), who reported the following concordance rates for Unipolar Depression in twins:
- MZ (identical) twins 40%
- DZ (non-identical) twins 11%
Whilst genetic makeup may predispose somebody to develop depression, a stressful life event might be needed to act as a trigger for that depression (diathesis-stress).
Neurotransmitters: The Monoamine Hypotheses
- Serotonin: responsible for regulation of mood, appetite and sleep
- Noradrenalin: Responsible for concentration and alertness
- Dopamine: Responsible for movement, memory, pleasure and a host of other functions.
You may have heard about serotonin’s role in depression before. One of serotonin’s main roles is the regulation of other neurotransmitters, so low levels of this neurotransmitter can lead to erratic brain functioning and thus distorted thinking. Low levels of serotonin also lead to imbalances in noradrenaline; another neurotransmitter implicated in depression. Low levels of serotonin can lead to changes in mood, appetite and sleep, whilst low levels of noradrenalin may lead to poor concentration and alertness. High levels of noradrenalin, on the other hand, has been implicated in mania (Schildkraut, 1965) thus suggesting that it may have a role in the highs of bipolar depression also. Low levels of dopamine can also result in sluggishness, lack of motivation and lack of alertness and focus.
Low levels of these monoamines have been implicated in depression, hence drug treatments are often used to correct these imbalances. A clinician will thus attempt to match the drug treatment to the symptoms shown by the patients, however several drug treatments may need to be tried for effectiveness, since different anti-depressants target different monoamines.
- + Teuting et al (1981) examined the urine of depressed patients and found chemicals that suggest lowered levels of both serotonin and noradrenalin.
- + The amino acid tryptophan is an essential pre-cursor of serotonin. A mutant gene that reduces levels of tryptophan, and results in an 80% reduction in serotonin levels, is ten times more likely to be found in depressed patients.
- – Drug therapies for Depression alter neurotransmitter levels almost immediately, yet it can take up to 6 weeks for patients to see a reduction in their symptoms. This indicates that neurotransmitter levels may be an indirect contributory factor. [The most recent theory for this is that high levels of cortisol in depressed patients kills off cells in the hippocampus, whilst SSRIs release neural growth hormone; it takes 4-5 weeks to repair this damage to the hippocampus (Nestler et al. 2001)]
Beck’s Cognitive Triad
Beck’s cognitive explanation of depression comprises three components: cognitive bias, negative self-schemas and the cognitive triad.
Beck discovered that those with depression tend to overexaggerate and focus on bad events, whilst downplaying or ignoring positive ones. They are prone to cognitive biases through the distortion and misinterpretation of events and situations. Beck described the main cognitives biases as:
- Arbitrary inference – drawing conclusions from insufficient/ no evidence.
- Selective abstraction – drawing conclusions from just one of many elements of a situation.
- Over-generalisation – making sweeping conclusions from a single event.
- Magnification – exaggerating the importance of an bad event.
- Minimisation – underplaying the importance of a positive event.
- Personalisation – attributing negative feelings of others to oneself.
A schema is a representation or model we create about aspects of ourselves and the world around us. They develop during childhood and onwards, based on our experiences. People with depression often create negative self-schemas based on information or criticism they may have received from parents, teachers or friends. A person with a negative self-schema is likely to employ the cognitive biases above.
The Cognitive Triad
Beck proposed that negative self-schemas and cognitive biases led to the cognitive triad; a negative view of ourselves, the world around us and the future.
Self: “I am worthless and inadequate.”
World: “Everybody hates me.”
Future: “I will never be good at anything.”
Ellis’ ABC (Irrational Thinking) Model
Ellis decided to define good mental health as ‘rational’ thinking and depression as ‘irrational’ thinking. Ellis’ ABC model proposes that an activating event leads to beliefs about that event, followed by consequences. This process can either be rational or irrational.
- A: Activating Event: A friend seems techy and snaps at you in class.
- B: Belief: A rational belief might be to assume that your friend is having a bad day, as this is not usual behaviour for them. An irrational belief might be that your friend now despises you as you are an unworthy human being.
- C: Consequence: A consequence of rational thinking might be that you give your friend some space for the day, or at lunchtime, gently ask them if they are ok. A consequence of irrational thinking thinking might be that you withdraw from the friendship and stop interacting with other people, believing that everyone hates you.
Evaluation of Cognitive Approach
- + A massive strength of the cognitive approach is the effectiveness of therapies based on this approach, such as Cognitive Behavioural Therapy (CBT) and Rational Emotive Behavioural Therapy (REBT, based on Ellis’ model). These treatments aim to change faulty thought processes to more positive ones and is relatively successful in helping people with depression. Success rates are usually around 40-50%.
- – It is not possible to establish cause and effect; are faulty thought processes the cause or effect of depression? It is possible that they are just a symptom.
- + Seligman’s research into ‘learned helplessness’ showed that animals (specifically dogs!) who could do nothing about their situation ‘learned’ to be helpless later on when they could do something about their situation. In Seligman’s research this was jumping over a divide to escape an electric shock. Dogs who had previously been unable to escape the fate of electric shocks, simply remained helplessly receiving shocks, even when they could do something about it. This research showed that the faulty cognitions associated with depression could be learnt.
- + Koster et al. (2005) examined the role of attention to negative stimuli in depression. It was found that depressed people took an average of 12ms to identify that a word was negative when it flashed up on a screen, compared to non-depressed students who only took 2ms. This supports Beck’s cognitive model as it shows that depressed people struggle to disengage from negative stimuli.
Cognitive-Behavioural Therapy (CBT)
Here are some great TED Talks to give you a better idea of what it is like to experience clinical depression.