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1.2 Mood (affective) disorders: depressive disorder (unipolar) and bipolar disorder

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1.2.1 Diagnostic criteria for mood (affective) disorders
(ICD-11 Criteria for disorders, types of episodes and Beck's Depression Inventory BDI)

↳ Key Study: Oruč et al. (1997)

↳ Example Study: Seligman et al. (1988)

Depressive Disorder: characterized by feeling sad, irritable, empty or a loss of pleasure. This is accompanied by other symptoms that affect an individual’s ability to function normally and conduct day-to-day tasks.

 

MANIC EP: at least a week where the mood is extremely high.

HYPOMANIC EP: a less extreme version of a manic episode involving several days of persistently elevated mood or increased irritability.

DEPRESSIVE EP: at least two weeks which involves depressed mood/lack of interest in usual activities for most of the day.

 

Intensity: Mania lasts a week whereas Hypomania is just around 4 days.

Impairment: Manic episode affects daily life and socializing whereas hypomania does not.

 

Bipolar Disorder: There are two types of this disorder.

Type 1: occurrence of at least 1 Manic Episode.

Type 2: occurrence of 1 or more hypomanic episodes and at least 1 depressive episode.

 

BECKS DEPRESSION INVENTORY (BDI 1996) Psychometric testing is a method of measuring personality traits, emotional states, or other experiences by using sets of questions and numerical scales.

This is a 21-item self-report measure that assesses attitudes and symptoms of depressive disorder and determines the severity of symptoms. It’s one of the most widely used tools for detecting depression. It can be used on people over the age of 13.

Scores: 14-19 = mild depression, 20-28 = moderate depression, 29-63 = severe depression.

(BDI relies on self-report data which is given during a semi-structured interview with a doctor. The doctor then completes the BDI based on the answers given. So, this means there can be interviewer effect, social desirability bias and overall validity is reduced)

 

EXPLANATIONS FOR MOOD DISORDERS:
BIOLOGICAL Biochemical:
 

Biological–biochemical: This explanation proposes that neurochemicals may cause depressive disorder. Schildkraut (1965) for example suggested that too much noradrenaline causes manic episodes and too little causes depressive episodes. It has also been found that both serotonin and noradrenaline imbalances are involved in mood (affective) disorders.

 

Monoamine Hypothesis: suggests that imbalances in neurotransmitters, specifically noradrenaline and serotonin, contribute to mood disorders. Initially focusing on noradrenaline, researchers noted that the drug reserpine, used for high blood pressure, induced depression by reducing noradrenaline levels. This led to the idea that noradrenaline deficiency might cause depression. Subsequently, attention turned to serotonin, which regulates noradrenaline levels. The hypothesis poses that an imbalance in serotonin could lead to fluctuations in noradrenaline levels, causing depressive or manic episodes. Together, noradrenaline and serotonin are referred to as monoamines in the context of this hypothesis.

KEY STUDY NAME: ORUČ ET AL. (1997) – 5-HT2C RECEPTOR AND 5-HT TRANSPORTER GENE FOR BIPOLAR DISORDER

 

Aim: To find out whether the genes encoding for 5-HHT and 5-HTR2c are associated with susceptibility to bipolar disorder.

 

Background: (Bipolar disorder ‘BP’ is characterized by episodes of elevated mood alternating with periods of depression.) There is a combination of biological and psychological factors associated with the onset of bipolar disorder.

Psychological factors like a breakdown of a relationship, or the death of a loved one. Or environmental factors like physical illness or sleep disturbance.

Biological factors refer to chemistry and genetics.

 

Main Theories Explained: Bipolar Disorder is 80% of the time most likely to be an inherited disorder. We know that noradrenaline, serotonin, and dopamine are all the neurotransmitters that are associated with BPD onset.

 

Method (Research method & design)

-Matched pairs design

-Clinical interviews

-Psychometric tests

-Blood/DNA analysis.

The control group matched patients in terms of age and sex

-Laboratory Experiment

 

Sample:

-Croatian

-Opportunity Sampling

-25 females and 17 males (T=42)

-Ages 31-70

-40 participants in the control group

-16 patients had a first-degree relative with a major affective mood disorder.

-All with BPD type 1 from the psychiatric hospitals in Zagreb, Croatia

 

Procedure:

  • All participants were interviewed (clinical interview) by a psychiatrist and given psychometric tests.

  • A clinical interview format is semi-structured (some standardised questions but flexibility for variation) and in this case, the technique was face-to-face.

  • For inter-rater reliability, all interviews were reviewed and confirmed by a second psychiatrist.

  • 16 participants (of the 42 with bipolar disorder) had a positive family history of mood (affective) disorders.

  • The diagnosis was confirmed by medical records which is an objective measure.

  • The same procedure was applied to the controls and all 40 had no history of mental ill-health.

  • Participants provided a blood sample and using the standardised procedure (a scientific, objective process) for extracting DNA (known as an ABI automated DNA synthesizer) the specific DNA polymorphisms were identified.

 

Results:

-Participants with BPD were not more likely to have polymorphisms of the genes.

Polymorphisms for genes

-Polymorphisms in these genes could be responsible for an increased risk of developing bipolar disorder in females only.

 

Conclusions:

Females may be more vulnerable to genetic alterations in the serotonergic transmission. Neither gene 5-TT nor the 5-HTR2c plays any role in the probability of developing BPD.

Sixteen of the participants had at least one first-degree relative who had a major affective disorder. In addition, polymorphisms in the genes of the participants could be responsible for the

increased risk of developing bipolar disorder

Strengths:

-Lab experiment means highly controlled and standardized leading to high levels of validity (internal)

-Used automated equipment which improves validity and removes researcher bias.

-Quantitative data gathered, easy to analyse.

Weaknesses:

-Limited sample size

-Gender bias 8 more females than males

-Age is an extraneous variable because some in the control group were able to get BPD but were too young for it to be developed.

Issues and Debates:

Nature versus nurture: Because of its focus on genetics, this study is an example of the nature side of the debate. Genes are passed from one generation to the next and so if a parent has depressive episodes, then the nature approach suggests that a person may inherit the genes that cause depressive episodes from a parent. The findings of the Oruč et al. study do not support this claim, but it is just one study with a limited focus. It does not mean that the nature explanation is wrong.

 

Reductionism versus holism: The limited focus mentioned above is that the study by Oruč et al. focused on the serotonin transmitters and serotonin receptors only, and so this is reductionist because it does.

not study other potential aspects of gene transmission and it does not consider the role of psychological factors that may cause depressive episodes. A more holistic approach would suggest that many factors including both biological and psychological factors should be taken into consideration.

 

Determinism versus free will: Focusing on genetics as the cause of depressive episodes is biological determinism. The Oruč et al. study does not consider free will at all. A cognitive explanation would be considered.

free-will.

PSYCHOLOGICAL EXPLANATIONS:

→ Becks Cognitive Triad: theorizes that depressed people have negative and hopeless thoughts or core beliefs about themselves, their experiences in the world, and their future.

Depressed people tend to distort and misinterpret information, a process known as cognitive bias. Beck, depressed people possess negative self-schemas, which may come from negative experiences, for example, criticism, from parents, peers or even teachers. Beck claimed that cognitive biases and negative self-schemas maintain the negative triad (shown above)

 

→Learned Helplessness:

Learned helplessness, developed by SELIGMAN (1960s), refers to a state that occurs after a person has experienced a stressful situation repeatedly. They believe that they are unable to control or change the situation, so they do not try, even when opportunities for change are available. Seligman proposed that learned helplessness could explain depressive disorders, suggesting that depression stems from a perceived lack of control over life circumstances.

This concept is foundational to the 'attributional style,' (attribution is the cognitive process by how people explain the causes of behaviours and events, our attributions may be biased or faulty) therefore this style is shaped by life experiences that influence how individuals interpret events. For example, someone with a history of challenges may develop a negative attributional style, consistently viewing negative events as internal, stable, and global - believing it's their fault (internal), expecting it to persist forever (stable), and anticipating many more problems now in various aspects of life (global).

 

EXAMPLE STUDY: SELIGMAN ET AL. (1988)

Aim: Seligman aimed to replicate research that showed a positive correlation between depressive attributional style and severity of depressive symptoms.

Sample: 51 patients (31 unipolar and 12 bipolar)

Methodology: Participants did the BDI and ASQ (attributional style questionnaire – asked questions about attributions to 12 hypothetical positive or negative events) Then they completed 6 months of weekly cognitive therapy. 32 were reassessed within a month of the last therapy session, and 26 followed up after 1 year. Findings compared with matched control group.

Results: 1- Positive correlation between depressive attributions for negative events and severity of symptoms before and after therapy. 2- Both bipolar and unipolar were found to have pessimistic, negative attributional styles. This means they tend to attribute negative events more to themselves (INTERNALALITY), they see negative things as more permanent (STABILITY) and believe that negative events affect many areas of their life (GLOBAL). 2- The more severe the depression score on the BDI, the worse the pessimism on the Attributional Style Questionnaire. 3- A substantial reduction in pessimism (a tendency to see the worst aspect of things or believe that the worst will happen.) during therapy corresponds to a greater improvement in depressive symptoms.

Conclusions: The study concluded that individuals with both types of mood disorders share a cognitive attributional style, but therapy can modify this tendency, increasing the likelihood of remission at 12 months.

TREATMENTS FOR MOOD DISORDERS:
BIOLOGICAL:

Antidepressant drugs are believed to affect the availability of monoamine neurotransmitters like serotonin, noradrenaline, and dopamine.

 

Tricyclics: Tricyclics alleviate depressive symptoms by blocking serotonin and noradrenaline transporter molecules in the presynaptic cell membrane, preventing the reabsorption of these neurotransmitters. Variations in effectiveness may be attributed to specific affinities for either serotonin or noradrenaline transporters. Although tricyclics bind to various receptors, this diversity is not believed to enhance their antidepressant effects and may contribute to certain side effects.

 

Monoamine Oxidase Inhibitors (MAOIs): Monoamine Oxidase Inhibitors (MAOIs) inhibit – to hinder or prevent – the activity of the enzyme monoamine oxidase, responsible for breaking down neurotransmitters like norepinephrine, serotonin, and dopamine. By inhibiting this breakdown, MAOIs elevate the levels of these neurotransmitters in the brain and allow them to remain at higher levels in the brain, thus improving mood. Despite evidence of effectiveness dating back to the 1950s, MAOIs come with significant side effects, including headaches, drowsiness/insomnia, nausea, diarrhoea, and constipation. Withdrawal issues and potential interactions with other medications, such as pain relievers and other antidepressants, can lead to negative effects like high blood pressure or headaches. Consequently, MAOIs are now typically reserved for treating depressive disorders only after other antidepressants or therapies have proven unsuccessful.

 

Selective serotonin reuptake inhibitors (SSRIs): These are a class of drugs that increase the availability of serotonin in the brain by binding to 5HT receptors on the cell. The drug binds to the serotonin transporter molecules on the presynaptic cell membrane, this binding prevents the reabsorption of released serotonin in the synapse, inhibiting the reuptake process.

 

TREATMENTS - PSYCHOLOGICAL:

Becks Cognitive Restructuring (1979)

Beck's cognitive restructuring is a talking therapy designed for individuals with depressive disorders. It involves one-to-one interactions where the therapist employs techniques like questioning to identify and change illogical thinking patterns. The therapy begins with explaining the theory of depressive disorder, including the cognitive triad, helping patients understand how their thoughts contribute to their depression. Patients are trained to observe and record their thoughts, allowing them to recognize irrational or inaccurate beliefs. The therapist guides them in understanding the link between thoughts, emotions, and behaviour. Patients practice identifying and recording automatic, dysfunctional thoughts in real-life situations. The therapy includes "reality testing" to explore negative thinking distortions. Techniques like "reattributing" help patients reframe situations and realize they may not be responsible for problems. The ultimate goal is for patients to independently use cognitive restructuring, leading to a reduction in depressive symptoms. Cognitive therapy has proven effective in managing depressive disorders, especially when drug treatment is unsuitable. Research shows its success in reducing symptoms for individuals not responding to antidepressants, with those receiving cognitive therapy being three times more likely to respond positively.

Ellis Rational Emotive Behaviour Therapy “REBT” (1962)

Musturbation: describes the way that some people allow 'the three musts' to control their thoughts, feelings, behaviour and ultimately their ability to enjoy life and contribute to society.

The three musts are: 1- People must approve of everything I do. 2- Other people must treat me well. 3- I must get what I want and not what I do not want.

Stoicism: a philosophy where one of the principles is that the individual is not directly affected by external things but by their perception of external things. Albert Ellis believed therapy should focus on the interpretation of events/situations rather than focusing on the event itself.

REBT was based on the principles of stoicism. This is the core of the theory on how a person becomes depressed due to their internal constructions. REBT helps individuals understand the ‘ABC’ model.

In REBT the therapist employs the ABC model, with the central focus on the beliefs (B) individuals hold about events. The key premise is that it is not the adversity itself, but rather one's thoughts about it, that significantly influences emotional well-being and behaviour. Persistent negative or irrational beliefs increase the risk of depressive disorder. The therapeutic goal is to help individuals cultivate constructive, rational thinking by identifying and changing thoughts leading to negative emotions and behaviours. The process of 'disputing' involves challenging irrational beliefs, enabling individuals to recognize their ability to control thoughts and feelings.

Studies, including a meta-analysis by Lyons and Woods, indicate that REBT leads to significant improvement over baseline measures and control groups. Comparative research suggests that REBT and antidepressants are equally effective in relieving symptoms of depressive disorder.

1.2.2 Explanations of mood (affective) disorders: depressive disorder (unipolar) (Biological - Genetic/Biochemical and Psychological)

1.2.3 Treatment and management of mood (affective) disorders (Biological - Antidepressants and Psychological - BCR/REBT)

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