1.5 - Mood (Affective) Disorders - Unipolar: Explanations
Introduction to depressive disorder
Depressive disorder, also known as unipolar depression, is a mood (affective) disorder characterised by persistent feelings of sadness, low mood, and loss of interest in activities. This can lead to symptoms such as changes in appetite, sleep disturbances, and difficulty concentrating. Understanding the causes of depression involves exploring both biological and psychological factors, which can interact to influence vulnerability and symptom severity.
Biological explanations of depression
Biological explanations focus on physical processes in the body and brain that may contribute to depression. These approaches suggest that imbalances in chemicals or genetic factors can increase the risk of developing the disorder.
Biochemical factors
Biochemical explanations propose that depression results from imbalances in certain neurotransmitters ~ chemical messengers that transmit signals between nerve cells in the brain. Low levels of specific neurotransmitters can disrupt mood regulation.
Key biochemical processes include:
- Noradrenaline - A neurotransmitter involved in alertness and energy; low levels are linked to feelings of fatigue and low mood in depression.
- Serotonin - Another neurotransmitter that helps regulate mood, sleep, and appetite; it also controls noradrenaline levels. An imbalance in serotonin can lead to decreased noradrenaline, causing depressive symptoms, or increased noradrenaline, potentially leading to mania (elevated mood states).
Serotonin deficiency may occur due to several factors:
- A diet low in tryptophan ~ an amino acid essential for producing serotonin.
- High levels of cortisol ~ a hormone released during stress that can interfere with serotonin production.
- Overly sensitive post-synaptic receptor sites ~ areas on receiving neurons that respond to neurotransmitters, which may overreact to low serotonin levels.
- High levels of monoamine oxidase ~ an enzyme that breaks down neurotransmitters like serotonin, reducing their availability.
- Abnormalities in presynaptic reuptake pumps ~ transporter molecules that recycle neurotransmitters back into the sending neuron, potentially leaving too little serotonin in the synapse (gap between neurons).
Genetic factors
Genetic explanations suggest that depression has a hereditary component, where certain genes increase vulnerability. This vulnerability is inherited through specific alleles ~ alternative forms of a gene.
For instance:
- Specific alleles related to serotonin pathways may heighten risk, especially when combined with stressful life events.
- Research shows that short alleles of the 5-HTT gene (which codes for serotonin transporter molecules) are associated with greater depression risk in stressful situations compared to long alleles, as found in studies like Caspi et al. (2003).
Key study: Oruč et al. (1997) on genetic factors in bipolar disorder
This study investigated genetic links to mood disorders, focusing on serotonin-related genes. Bipolar disorder involves both depressive and manic episodes, providing insights into unipolar depression as well.
Aim
- To examine if specific alleles of the 5-HTR2c and 5-HTT genes are more common in people with bipolar disorder compared to controls.
- The 5-HTR2c gene codes for post-synaptic receptors linked to appetite regulation, often affected in depression, while the 5-HTT gene codes for presynaptic transporter molecules.
Participants
- An opportunity sample of 82 adults from Croatia, including 42 with bipolar disorder and a matched control group.
Method
- A correlational design using interviews and blood tests to collect data.
- Co-variables included bipolar diagnosis and presence of specific alleles (Cys (C) or Ser (S) for 5-HTR2c; 1 or 2 for 5-HTT).
Procedure
- Participants were diagnosed via interviews and medical records.
- Blood samples determined alleles.
- Controls were matched for age and sex, and diagnoses were verified by psychiatrists.
Results
- In the bipolar group, 38% had at least one first-degree relative with a mood disorder, compared to 0% in controls.
- The S and 1 alleles were more frequent in diagnosed females than healthy female controls.
Conclusions
- Variants like S and 1 alleles of the 5-HTR2c and 5-HTT genes may increase depression risk, particularly in females.
Evaluation
| Strengths | Weaknesses |
|---|---|
| Validity - Diagnoses were confirmed by two psychiatrists using a structured interview, enhancing accuracy. | Generalisation - Small sample size, with only three males having the SS genotype, limits broader applicability. |
| Reliability - Findings align with other studies (e.g., Gutiérrez et al., 1996; Kelsoe et al., 1996). | Validity - Correlational design prevents establishing cause and effect; groups were only matched on age and sex. |
Ethical considerations included maintaining confidentiality of medical records and obtaining informed consent for blood tests and record access.
Psychological explanations of depression
Psychological explanations emphasise how thought patterns and learned behaviours contribute to depression. These approaches suggest that negative experiences shape cognition, leading to persistent low mood. They contrast with biological views by focusing on modifiable mental processes.
Beck's cognitive theory
Beck's cognitive theory (1962) argues that depression stems from dysfunctional core beliefs deeply held ideas about oneself and the world which lead to negative thoughts and symptoms. The more negative these thoughts, the more severe the depression.
Key elements include:
- Negative cognitive triad - Depressed individuals hold pessimistic views about the self (e.g., "I am worthless"), the world (e.g., "Life is unfair"), and the future (e.g., "Things will never improve").
- These beliefs often form in childhood due to experiences like criticism, rejection, neglect, abuse, bullying, loss, or overprotective parenting.
- Faulty thinking strategies maintain depression, such as:
- Confirmation bias - Focusing on evidence that supports negative beliefs while ignoring positive information.
- Catastrophising - Exaggerating the importance of negative events.
- Personalising - Assuming responsibility for events not under one's control.
Learned helplessness and attributional style
Learned helplessness theory suggests depression develops as a response to uncontrollable negative experiences, leading to passive behaviour. If a neutral stimulus becomes linked with an unavoidable negative outcome, individuals may stop trying to cope in similar future situations.
This leads to:
- Feelings of hopelessness and overgeneralisation, where lack of control in one area extends to others.
- Depressive attributional style - A pessimistic way of explaining events, involving biases in processing success and failure.
Relevant research: Seligman et al. (1988) on attributional style
This study explored the link between depressive attributional style and symptom severity, building on learned helplessness theory.
Aim
- To replicate findings of a positive correlation between pessimistic attributions and depressive symptoms, and assess changes after therapy.
Participants
- Mood-disordered individuals, with 50% more females than males, compared to a matched control group.
Method
- Participants completed the Beck Depression Inventory (BDI) - a questionnaire measuring depression severity - and an attribution questionnaire for 12 events.
- Diagnoses were confirmed via interviews, with reassessments after six months of cognitive therapy and at one- and 12-month follow-ups.
Results
- Pessimistic attributions for negative events correlated with higher depressive symptoms before and after therapy.
- Greater reductions in pessimism post-therapy led to symptom improvement, which remained stable. Post-therapy pessimism predicted relapse at 12 months.
Conclusions
- Mood disorders involve internal, global, and stable attributions for negative events, but therapy can modify this style.
Evaluation
| Strengths | Weaknesses |
|---|---|
| Validity - Pessimism was stable in controls, suggesting it's a trait causing depression, not a symptom. | Generalisation - Female-heavy sample may not represent all males with depression. |
| Validity - Triangulation via BDI and interviews improved measurement accuracy. | Attrition - 33% dropout by final follow-up; remaining participants might have milder symptoms. |
Strengths and weaknesses of explanations
Each explanation has supporting evidence and limitations, as summarised below:
| Approach | Explanation | Strengths | Weaknesses |
|---|---|---|---|
| Biological | Biochemical | Evidence - Reducing tryptophan in diets increased depressive symptoms in vulnerable people. Applications - Led to drug treatments improving daily functioning. | Evidence - Low serotonin might result from depression (e.g., in submissive monkeys). Deterministic - Assumes uniform responses to neurotransmitter changes. |
| Biological | Genetic | Evidence - Higher concordance in monozygotic (MZ) twins (38%) vs dizygotic (DZ) twins (14%). Applications - Could enable personalised treatments via pharmacogenomics. | Validity - Shared environments in twin studies confound results. Reliability - Genome-wide association studies show inconsistent gene patterns. |
| Psychological | Beck's cognitive theory | Scientific - Allows testable hypotheses, e.g., on confirmation bias in depressed vs non-depressed people. | Overly deterministic - Some regain control through therapy, exercising free will. |
| Psychological | Learned helplessness/attributional style | Evidence - Seligman et al. (1988) showed correlations and therapy benefits. | Bidirectional ambiguity - Pessimism might be a symptom, not a cause, of depression. |
Issues and debates in explanations of depression
Explanations of depression raise broader questions about human behaviour and mental health. These debates help evaluate the completeness of different approaches.
Nature versus nurture
This debate considers whether depression is primarily inherited (nature) or shaped by environment (nurture). Twin studies support nature, showing higher concordance in MZ twins. However, adoption studies are mixed: Kendler et al. (2018) found increased risk in adoptive children with depressed adoptive parents (nurture), while Mendlewicz and Rainer (1977) showed higher rates in biological parents of adopted children with bipolar (31%) compared to adoptive parents (12%) (nature).
Oruč et al. (1997) emphasises nature through genes, whereas Seligman et al. (1988) highlights nurture via learned attributions.
Reductionism versus holism
Reductionism breaks depression down to single factors, like genes in Oruč et al. (1997), ignoring epigenetics ~ environmental influences on gene expression.
Holistic views, such as the diathesis-stress model, integrate biological vulnerabilities (diathesis) with environmental stressors, offering a more complete explanation.
Determinism versus free will
Psychological explanations may be seen as overly deterministic. However, individuals may exercise free will through therapy to change negative patterns, challenging this view.