Depression

Introduction

Depression (major depressive disorder, MDD) is a mood disorder characterised by persistent low mood, Loss of interest or pleasure in activities (anhedonia), disturbances in sleep and appetite, fatigue, Difficulty concentrating, feelings of worthlessness or excessive guilt, and in severe cases, Suicidal ideation. Depression is one of the most common mental disorders, affecting approximately 3.8% of the global population, and is a leading cause of disability worldwide.

Biological Explanations

Genetic Factors

Family, twin, and adoption studies consistently demonstrate that depression has a heritable Component. The heritability of major depression is estimated at approximately 0.37 (Sullivan, Neale, And Kendler, 2000), indicating that genetic factors account for approximately 37% of the variance in Liability to depression, with the remaining variance attributable to environmental factors.

Twin studies: MZ twins show a concordance rate for depression of approximately 40—50%, compared To approximately 20—25% for DZ twins. The difference in concordance rates between MZ and DZ twins Supports a genetic contribution, but the fact that MZ concordance is well below 100% demonstrates That non-shared environmental factors also play a major role.

Candidate genes: Several genes have been implicated in depression, including the serotonin Transporter gene (5-HTTLPR), the brain-derived neurotrophic factor (BDNF) gene, and genes involved In the hypothalamic-pituitary-adrenal (HPA) axis. However, no single gene has a large effect; Depression is a polygenic disorder influenced by many genes, each with a small effect.

Neurotransmitter Theories

The monoamine hypothesis: The monoamine hypothesis of depression proposes that depression is Caused by a deficiency in monoamine neurotransmitters, particularly serotonin (5-HT), norepinephrine (NE), and dopamine (DA). This hypothesis was initially based on the observation that drugs that Deplete monoamines (e.g., reserpine) can cause depressive symptoms, while drugs that increase Monoamine availability (e.g., MAO inhibitors, tricyclic antidepressants) have antidepressant Effects.

The serotonin hypothesis: A specific version of the monoamine hypothesis focuses on serotonin. Low levels of serotonin (or reduced serotonin receptor sensitivity) are hypothesised to cause Depression. This hypothesis is supported by the effectiveness of SSRIs (selective serotonin reuptake Inhibitors) in treating depression, which increase serotonin availability in the synaptic cleft.

Evaluation of neurotransmitter theories:

• The monoamine hypothesis is supported by the pharmacological evidence, but it is incomplete. SSRIs increase serotonin availability within hours, but their therapeutic effects take 2—4 weeks to develop, suggesting that the antidepressant mechanism involves downstream changes (e.g., neuroplasticity, BDNF expression) rather than correcting a neurotransmitter deficit.
• The hypothesis cannot explain why some individuals with normal neurotransmitter function develop depression, nor why some individuals with low neurotransmitter function do not.
• Kirsch et al. (2008) conducted a meta-analysis of clinical trials of antidepressants (including SSRIs) and found that the difference between drug and placebo was clinically significant only for patients with very severe depression. For mild to moderate depression, the drug-placebo difference was small and possibly not clinically meaningful.

The HPA Axis and Neuroendocrine Factors

The hypothalamic-pituitary-adrenal (HPA) axis is the body”s primary stress response system. In Response to stress, the hypothalamus releases corticotropin-releasing hormone (CRH), which Stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH), which in turn Stimulates the adrenal cortex to release cortisol.

HPA axis hyperactivity in depression: Many individuals with depression show elevated cortisol Levels (hypercortisolism), enlarged adrenal glands, and impaired negative feedback regulation of the HPA axis. The dexamethasone suppression test (DST) demonstrates that approximately 50% of Individuals with major depression fail to suppress cortisol production in response to dexamethasone (a synthetic glucocorticoid), indicating HPA axis dysregulation.

Mechanism: Chronic stress leads to sustained activation of the HPA axis, resulting in elevated Cortisol levels. Chronic cortisol elevation damages hippocampal neurons (through excitotoxicity and Reduced BDNF expression), impairing the hippocampus’s ability to regulate the HPA axis through Negative feedback. This creates a vicious cycle: stress causes HPA axis activation, cortisol damages The hippocampus, impaired hippocampal function further impairs HPA axis regulation, leading to more Cortisol release.

Cognitive Explanations

Beck’s Cognitive Triad (1967)

Aaron Beck proposed that depression is caused by systematic negative patterns of thinking. The core Of Beck’s theory is the cognitive triad: three types of negative beliefs about the self, the World, and the future.

1. Negative views about the self: “I am worthless,” “I am a failure,” “I am unlovable.” The individual believes they are fundamentally deficient.
2. Negative views about the world: “The world is unfair,” “People are against me,” “Nothing ever goes right.” The individual interprets experiences through a negative filter.
3. Negative views about the future: “Things will never get better,” “There is no hope,” “Nothing I do will make a difference.” The individual expects continued suffering and failure.

Cognitive distortions: Beck identified specific patterns of biased thinking that maintain the Cognitive triad:

• Arbitrary inference: Drawing negative conclusions without evidence (e.g., “She didn’t smile at me; she must dislike me”).
• Selective abstraction: Focusing exclusively on negative details while ignoring positive information.
• Overgeneralisation: Drawing a general conclusion from a single negative event (e.g., “I failed this exam; I will fail at everything”).
• Magnification and minimisation: Exaggerating the significance of negative events and minimising the significance of positive events.
• Personalisation: Attributing negative events to oneself when there is no basis for doing so.
• Dichotomous (all-or-nothing) thinking: Seeing things in black-and-white categories (e.g., “If I am not perfect, I am a total failure”).

Evaluation of Beck’s theory:

• The theory has strong empirical support. Depressed individuals do show more negative automatic thoughts and cognitive distortions than non-depressed individuals, as measured by the Dysfunctional Attitudes Scale and the Automatic Thoughts Questionnaire.
• The theory forms the basis of cognitive-behavioural therapy (CBT), which is one of the most effective treatments for depression.
• However, the direction of causality is debated. Do negative cognitions cause depression, or does depression cause negative cognitions? Longitudinal studies (e.g., Lewinsohn, Steinmetz, Larson, and Franklin, 1981) have provided evidence for both directions: negative cognitions predict the onset of depression, but depression also increases the frequency of negative cognitions, suggesting a reciprocal relationship.

Learned Helplessness and Attributional Style

Seligman (1975): Martin Seligman developed the learned helplessness model based on experiments With dogs. Dogs subjected to inescapable electric shocks (in which no response could terminate the Shock) later failed to escape from shocks in a situation where escape was possible. Seligman argued That the dogs had “learned” that their actions had no effect on outcomes, and this learned Helplessness generalised to new situations.

Abramson, Seligman, and Teasdale (1978): The reformulated learned helplessness model applied the Concept to human depression and introduced the concept of attributional style. When people Experience negative events, they make causal attributions along three dimensions:

1. Internal versus external: Is the cause due to me (internal) or to external circumstances?
2. Stable versus unstable: Is the cause permanent (stable) or temporary (unstable)?
3. Global versus specific: Does the cause affect all areas of my life (global) or just this particular situation (specific)?

A pessimistic attributional style (attributing negative events to internal, stable, and global Causes: “I failed because I am incompetent, and I will always be incompetent at everything”) is Associated with vulnerability to depression. An optimistic attributional style (attributing negative Events to external, unstable, and specific causes) is protective.

Evaluation:

• The reformulated model is well-supported by research. Pessimistic attributional style predicts the onset of depression in prospective studies (Alloy et al., 2006).
• The model explains individual differences in vulnerability to depression: two people may experience the same negative event, but only the person with a pessimistic attributional style is likely to become depressed.
• However, not all individuals with pessimistic attributional styles develop depression, and not all individuals with depression have pessimistic attributional styles. Attributional style is one vulnerability factor among many.

Sociocultural Explanations

Social Stress and Life Events

Stressful life events (e.g., bereavement, relationship breakdown, job loss, financial difficulties) Are among the most robust predictors of depression onset. Brown and Harris (1978) found that women Who experienced a severe life event accompanied by a “negative evaluation” (e.g., humiliation, Entrapment) were significantly more likely to develop depression.

Socioeconomic Status

Depression is more prevalent among individuals of lower socioeconomic status (SES). Poverty, Unemployment, inadequate housing, food insecurity, and lack of access to healthcare all contribute To chronic stress, which increases vulnerability to depression. The relationship between SES and Depression is bidirectional: low SES increases the risk of depression, and depression impairs Educational and occupational functioning, potentially perpetuating low SES.

Gender Differences

Women are approximately twice as likely as men to be diagnosed with depression. Proposed Explanations include:

• Biological factors: Hormonal fluctuations (menstrual cycle, postpartum period, menopause) may contribute.
• Social role explanations: Women are more likely to experience chronic stressors such as domestic violence, caregiving burdens, and workplace discrimination.
• Rumination: Women are more likely than men to ruminate on their negative emotions, which prolongs and intensifies depressive episodes (Nolen-Hoeksema, 1991).
• Diagnostic bias: Women may be more likely to seek help and receive a diagnosis, while men’s depression may go unrecognised or be expressed as anger or substance abuse.

Treatments

Pharmacological Treatment: SSRIs

Selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine (Prozac), sertraline (Zoloft), And escitalopram (Lexapro), are the most commonly prescribed antidepressants. SSRIs work by blocking The serotonin transporter (SERT), increasing the concentration of serotonin in the synaptic cleft.

Effectiveness: SSRIs are moderately effective for moderate to severe depression. Meta-analyses (Cipriani et al., 2018) have found that all commonly prescribed antidepressants are more effective Than placebo, but the effect sizes are modest (approximately 0.3 standard deviations).

Kirsch et al. (2008): Analysed data from 35 clinical trials submitted to the FDA and found that The difference between SSRI and placebo was not significant for patients with mild or moderate Depression (effect size less than 0.2). For severe depression, the drug-placebo difference was Larger but still modest. This finding suggests that a significant proportion of the SSRI’s Therapeutic effect may be attributable to placebo effects.

Side effects: SSRIs can cause nausea, insomnia, sexual dysfunction, weight gain, and emotional Blunting. SSRIs carry an FDA “black box” warning for increased risk of suicidal ideation in Children, adolescents, and young adults (under age 25).

Psychological Treatment: Cognitive-Behavioural Therapy (CBT)

CBT for depression, developed by Beck, aims to identify and modify the negative automatic thoughts, Cognitive distortions, and core beliefs that maintain the cognitive triad. CBT involves:

1. Cognitive restructuring: Identifying negative automatic thoughts and challenging them with evidence.
2. Behavioural activation: Encouraging the individual to engage in pleasurable or meaningful activities that they have been avoiding due to depression.
3. Skills training: Teaching coping skills, problem-solving skills, and social skills.

Effectiveness: CBT is at least as effective as pharmacotherapy for mild to moderate depression (Hollon et al., 2005) and may be more effective than pharmacotherapy in preventing relapse. Combination therapy (CBT plus antidepressants) may be more effective than either treatment alone for Severe depression.

Combination Therapy

For severe depression, the combination of pharmacotherapy and psychotherapy is often recommended. Elkin et al. (1989) conducted the NIMH Treatment of Depression Collaborative Research Program, Comparing CBT, interpersonal therapy (IPT), imipramine (a tricyclic antidepressant), and placebo. For severely depressed patients, both CBT and imipramine were more effective than placebo, and Combination approaches showed the greatest improvement.

For an overview of abnormal psychology topics, see Abnormal Psychology.

Common Pitfalls

1. Confusing correlation and causation in psychological research evidence.

2. Stating that ‘the results show’ without considering whether the findings can be generalised beyond the sample.

3. Presenting theories without the supporting empirical evidence that led to their acceptance.

4. Describing a study without evaluating its methodology (e.g., sample, controls, ecological validity).

Summary

The key principles covered in this topic are linked in the sub-pages above. Focus on understanding the definitions, applying the formulas or frameworks, and evaluating strengths and limitations of each approach.

Worked Examples

Worked examples demonstrating the application of key concepts are covered in the detailed sub-pages linked above.