Unipolar Depression (Edexcel A-Level Psychology): Revision Notes

Unipolar Depression Overview

Introduction

Major depressive disorders belong to the broader category of mood disorders, conditions that alter how individuals experience themselves and interact with the world around them. There are two primary forms of mood disorder: unipolar depression and bipolar disorder. Bipolar disorder involves alternating periods of manic episodes (elevated mood) and depressive episodes, whereas unipolar depression is characterised by persistent low mood alongside other symptoms. Importantly, unipolar depression encompasses several subtypes that vary in severity, duration, and whether the condition has psychotic features.

Symptoms

Depression cannot be diagnosed through physiological testing alone; instead, diagnosis relies heavily on clinical expertise and the identification of specific symptom patterns. The symptoms of depression span four main categories: emotional, somatic, motivational, and cognitive.

Emotional symptoms relate to subjective mood states. In major depression, individuals typically experience persistently low or negative mood. This encompasses feelings of sadness, hopelessness, and an inability to experience pleasure or interest in activities previously enjoyed.

Somatic symptoms involve alterations to physical and physiological functioning. These include changes in sleeping patterns (either insomnia or hypersomnia), significant weight loss or gain, observable psychomotor agitation (restlessness) or retardation (slowed movement), fatigue, and changes in appetite.

Motivational symptoms concern behavioural patterns and the individual's willingness to engage with the world. People with depression often lack the persistence or determination to achieve goals. If an individual feels apathetic, they are less likely to initiate activities or maintain effort towards completing tasks.

Cognitive symptoms reflect systematic alterations in how the person processes information, leading to negative interpretations of their circumstances. These include difficulty concentrating, feelings of worthlessness or excessive inappropriate guilt, and recurrent thoughts of death or suicidal ideation.

DSM-V diagnostic criteria

Features

Age of onset and course

Unipolar depression can emerge at any age, though it appears more frequently during young adulthood. The progression and severity of the disorder vary considerably between individuals. Some people may appear to function relatively well, whilst others may experience remission within a few months of onset and remain symptom-free thereafter. However, for individuals with personality disorders or high levels of anxiety, symptoms can be severe and enduring, with limited periods of remission.

Risk factors

The likelihood of developing major depression is influenced by temperament. Neuroticism—emotional instability characterised by anxiety, fear, depression, and envy—represents a well-established risk factor, particularly when paired with stressful life circumstances. Risk increases for those who have experienced negative events during childhood or who have a first-degree relative with the disorder.

Mortality

Major depressive disorder is associated with elevated mortality rates, predominantly through suicide, though it also affects the progression of other illnesses. Suicide rates are higher amongst male sufferers, but females attempt suicide more frequently. The risk of suicide increases when the individual is single, lives alone, and experiences strong feelings of hopelessness.

Prevalence

Unipolar depression has a relatively high prevalence rate (the proportion of a population affected at any given time), though this varies across cultures. The DSM estimates a rate of 7% in the USA, though this figure is likely higher amongst those aged 18–29 years. There is a substantially higher incidence in females, with female sufferers outnumbering males by at least a two-to-one ratio. These cultural and gender variations may reflect differences in how depression is diagnosed and reported, rather than straightforward links between culture, gender, and the disorder itself.

Biological explanation

Biological accounts of depression centre on genetics, abnormalities in neurotransmitter systems, and hormonal influences. These explanations also consider anatomical changes in brain regions such as the prefrontal cortex and limbic system, with recent research investigating the role of the hippocampus.

The role of neurotransmitters

Serotonin is a chemical messenger responsible for regulating mood. Noradrenaline (also called norepinephrine) is a catecholamine hormone and neurotransmitter involved in multiple functions, including maintaining concentration.

However, whilst levels of noradrenaline and serotonin rise within hours of administering antidepressant medication, symptoms frequently do not improve for a period of up to two weeks in some cases. This delay challenged the straightforward monoamine hypothesis and prompted the development of alternative explanations.

One refined explanation suggests that low levels of noradrenaline and serotonin lead to alterations in the brain's neural circuitry, specifically causing increased sensitivity (up-regulation) of receptor sites—areas on the postsynaptic neuron that permit neurotransmitters to bind to the membrane. With insufficient serotonin and noradrenaline, there is inadequate stimulation of postsynaptic receptors. To compensate, additional receptors are produced, increasing the neurotransmitter's availability at the synapse through antidepressant administration. However, there is then a down-regulation process, wherein the brain reduces receptor production in response to increased neurotransmitter levels. This homeostatic mechanism can explain the delay in therapeutic effect, as this adjustment process interferes with immediate symptom relief.

Alternative explanations for depression: cortisol

Depression is consistently linked to abnormalities in the neuroendocrine system, particularly the hypothalamic-pituitary-adrenal (HPA) axis, which regulates the body's stress response through cortisol release from the adrenal cortex. A key structure in this system is the hippocampus, which controls the levels of corticotrophin-releasing hormone (CRH), leading to cortisol production and release.

Typically, a negative feedback mechanism deactivates CRH production once cortisol levels rise. However, in cases of severe stress and depression, this mechanism fails, resulting in persistently elevated cortisol in the bloodstream. High cortisol levels negatively affect the hippocampus, leading to increased CRH release and creating a harmful cycle with sustained stress hormone production.

Evaluation of biological explanations

Much of the evidence supporting the role of serotonin and noradrenaline in depression derives from drug research. Serotonin mediates mood, and reduced serotonin levels may contribute to depression. MDMA (ecstasy), an illegal recreational drug, increases serotonin release into the synaptic gap and is associated with feelings of euphoria (intense happiness). Many antidepressant medications work by blocking serotonin reuptake, making it available in the synaptic gap for postsynaptic receptor uptake, thereby elevating mood. Given the robust biological evidence for low serotonin causing depression, some researchers maintain that antidepressants produce a placebo effect, which may account for mood improvement in many patients (Kirsch et al., 2002).

Recent research has raised doubts about serotonin's role in depression. Mariana Angoa-Pérez and colleagues (2014) bred mice lacking the gene for tryptophan, an enzyme essential for serotonin production. These mice showed no signs of depression across multiple tests and were unresponsive to antidepressant medication. Even when subjected to stress, the mice responded no differently from normal mice. This evidence suggests depression's cause extends beyond low serotonin levels and that other factors must be implicated. However, caution is necessary when generalising findings from animal studies to human depression.

A recent meta-analysis by Sullivan, Neale, and Kendler (2000) examined family, twin, and adoption studies investigating heredity's role in major depression. They found a familial transmission of depression, with a 40% increased risk of developing the disorder when a first-degree relative has it (according to DSM-V statistics). This could indicate a genetic vulnerability to neurotransmitter dysfunction.

Non-biological explanation: a cognitive behavioural theory

Operant conditioning

Behaviourist theories explain depression as resulting from environmental factors causing faulty learning, which establishes maladaptive behavioural responses. Lewinsohn (1974) proposed that depression occurs due to insufficient positive reinforcement (rewarding outcomes for behaviour) from the environment. Individuals either fail to engage with their social environment or lack the social skills necessary to obtain reinforcement. For instance, if someone is socially awkward, their conversational attempts might be ignored. This lack of reinforcement contributes to feelings of worthlessness and withdrawn behaviour characteristic of depression symptoms.

Whilst extrapolating animal research to complex human behaviour like depression may be challenged due to humans' higher cognitive functioning, the research has been successfully replicated in humans. However, not all dogs responded identically; if the behaviour were purely learned, all dogs should respond to the same environmental stimuli identically. This suggests a cognitive element to the explanation more specifically related to humans.

Cognition

Abramson (1978) refined the behaviourist explanation to incorporate a cognitive component, specifically the attributional bias—how we habitually locate causes for events. People with a maladaptive attributional style (faulty behaviour we commonly exhibit) tend to emphasise fault within themselves as a causal factor for their failures. They internalise failure, suggesting they cannot change and that failure will affect everything they undertake. This is termed an internal, stable, and global attribution of failure. Non-depressed individuals are more likely to attribute failure to external factors, temporary circumstances, or situation-specific events.

Beck (1967, 1976) developed a more cognitive-based explanation, arguing that depression and depressed mood result from pessimistic schema—core information and beliefs about how the world functions. Negative schema (habitual self-critical and damaging thought patterns) develop during childhood from early trauma and unhappy experiences, creating a cognitive triad of beliefs about: themselves (seeing themselves as worthless and useless); their environment (perceiving it as overwhelming and obstacle-filled); and their future (viewing it as hopeless).

When confronted with stress, individuals with these negative schema apply faulty logic in interpreting events. These interpretations can be described as cognitive distortions, which alter perception and trigger anxiety and negative emotions, subsequently triggering behaviour consistent with depression symptoms, such as passivity and helplessness.

Beck identified several types of cognitive distortion:

Cognitive distortion	Example
Polar reasoning (also known as "all or nothing" thinking)	Unless everything is absolutely perfect, it is considered a complete failure, e.g., a student receives an A instead of an A* and feels worthless as a result
Selective abstraction	Ignoring positive aspects in favour of focusing on minor negative elements that can be interpreted negatively. Success is disregarded and the person recalls only failure, e.g., a student receives 8 A*s and a D grade, and they focus on the D grade, which is magnified in their mind
Overgeneralisation	One minor aspect of an experience is extrapolated to form a belief about what happened, e.g., failure on one essay means that failure on the course is inevitable

These cognitive distortions alter perception and trigger anxiety and negative emotions, which subsequently trigger behaviour consistent with depression symptoms.

Evaluation of cognitive theories

The main limitation of the behaviourist model of depression, such as Lewinsohn's, is its failure to explain the root causes of depression. Poor social interactions or isolation limiting reinforcing experiences might be a cause or symptom of depression. Similarly, the learned helplessness perspective cannot explain why someone would become suicidal, as it predicts passive acceptance of the situation rather than an active desire to die—a depression symptom. Additionally, it struggles to explain cases of endogenous depression, as behaviourist theories require an environmental contribution, which is not evident in some endogenous depression cases.

The cognitive behavioural approach addresses some of these limitations by suggesting that a pessimistic explanatory style leads to depression. However, it remains unclear how this develops, and whilst it may contribute to symptom maintenance, it might not be the primary cause.

Lewinsohn et al. (2001) researched adolescent depression, finding that when stressed, dysfunctional attitudes rather than environmental factors (as suggested by the learned helplessness model) were the strongest predictor of adolescent major depressive disorder. Other studies demonstrate links between negative thinking and depression, though there is limited evidence conclusively showing that negative thinking preceded depression onset, as Beck's theory suggests. It also fails to explain the gender bias, with women suffering more frequently than men, as there is no evidence suggesting females have more negative schema than males.

An alternative perspective argues that negative thinking is actually perfectly reasonable, termed "depressive realism." People with good mental health may be less realistic (or more pessimistic) in their thought processes, viewing the world through rose-tinted glasses. A depressed person is simply a realist.

Regardless of whether faulty thinking is a causal factor, it remains an effective therapeutic approach. Cognitive behavioural therapy has demonstrated effectiveness in reducing symptoms in many studies, such as Kuyken et al. (2007), suggesting some validity to the theory.

Individuals may be more vulnerable to depression if certain life events occur that trigger a genetic predisposition. Brown and Harris (1978) studied depressed women in a London area, finding that major life events tended to occur before a depression episode. They also established that certain factors, such as lack of external employment, having young children, and chronic life difficulties, contributed to depression. However, establishing a causal relationship is difficult because depression may precipitate loss of employment or other major life difficulties.