DP explanations

Bio and Cog explanation

What is the monoamine hypothesis of depression?

It states that depression is caused by low levels of certain neurotransmitters in the brain, primarily serotonin, noradrenaline, and dopamine.

How does low noradrenaline relate to depressive symptoms?

Low noradrenaline is linked to a lack of pleasure (anhedonia) and can cause dopamine levels to drop, which is associated with anxiety.

What is serotonin’s proposed role in the monoamine hypothesis?

Serotonin is thought to regulate the levels of other neurotransmitters (noradrenaline and dopamine); low serotonin may lead to dysregulation of these systems.

What happens in the synapse when serotonin or noradrenaline levels are chronically low?

The postsynaptic neuron may undergo downregulation—producing fewer receptors to compensate for reduced stimulation.

Why might antidepressant effects take several weeks to appear?

Because neurochemical changes like receptor up/downregulation and synaptic remodeling are gradual processes that correlate with symptom improvement.

What other problem besides low neurotransmitter levels could cause depression?

Faulty or insufficient postsynaptic receptors, leading to poor signal transmission even if neurotransmitter levels are adequate.

What are the two main ways serotonin is cleared from the synapse?

1. Reuptake (reabsorption into the presynaptic neuron) 2. Enzymatic breakdown (by MAO-A).

How could overly active reuptake contribute to depression?

If reuptake is 'too fast,' serotonin is pulled back into the neuron too quickly, reducing its availability in the synaptic gap.

How could excessive MAO-A activity contribute to depression?

High levels of MAO-A break down serotonin (and other monoamines) too rapidly, starving the brain of these neurotransmitters.

What was the first known antidepressant, and how was it discovered?

Isoniazid, originally a tuberculosis drug, was found to cause euphoria as a side effect, leading to the discovery that it inhibits MAO.

How do MAO inhibitors (MAOIs) work?

They block the enzyme monoamine oxidase (MAO-A), increasing levels of serotonin, noradrenaline, and dopamine in the synapse.

What are the risks of excessive MAO inhibition?

Can lead to overly high monoamine levels, causing agitation, aggression, psychosis, and dangerous side effects like hypertensive crisis.

What percentage of patients typically respond to traditional antidepressants?

About 60–80% of patients experience relief.

What are common reasons for non-adherence to antidepressant medication?

Side effects, emotional blunting, forgetting, or feeling well and stopping prematurely.

What significant limitation does non-response to antidepressants suggest?

Not everyone’s depression is purely neurochemical; other factors must be considered.

What is the permissive hypothesis?

It suggests that low serotonin 'permits' other neurotransmitter systems to become dysregulated, leading to depression.

What is the stress-diathesis model in depression?

It proposes that genetic predisposition interacts with environmental stressors to trigger depressive episodes.

Which gene is frequently linked to serotonin regulation and depression risk?

The 5-HTT gene (serotonin transporter gene).

What is BDNF and what role does it play in the brain?

A protein that supports neuroplasticity—the growth, survival, and function of neurons.

How are BDNF levels related to depression?

Lower BDNF levels are correlated with more severe depressive symptoms.

What did Sen et al. (2008) find regarding BDNF?

A negative correlation between blood serum BDNF levels and depression severity.

What did Martinowich et al. (2007) discover in post-mortem studies?

Abnormally low BDNF levels in the hippocampus and prefrontal cortex of people who had depression.

How might stress affect BDNF?

Chronic stress may 'switch off' the BDNF gene, leading to neuron atrophy or apoptosis.

What is a key reductionist critique of neurochemical theories?

They oversimplify depression to chemical imbalances, ignoring cognitive, emotional, social, and environmental factors.

Why might antidepressants’ delayed onset challenge the monoamine hypothesis?

If depression were solely due to low neurotransmitter levels, correcting them should bring immediate relief—but improvement takes weeks.

How does the cognitive explanation complement biological theories?

It addresses psychological processes that may interact with or precede neurochemical changes.

What does the variability in antidepressant response imply?

Depression is likely heterogeneous—different subtypes may have different underlying causes.

What is the core assumption of Beck’s cognitive theory of depression?

That depression is caused and maintained by faulty or irrational thinking patterns.

How do faulty cognitions contribute to a 'downward spiral' in depression?

Negative thoughts lead to negative feelings, reinforcing negative perceptions and behaviors.

What are the three components of Beck’s negative cognitive triad?

1. Negative view of the self 2. Negative view of the world 3. Negative view of the future.

How do these three components interact?

They reinforce each other—e.g., feeling worthless leads to expecting failure in the future.

What is a schema in Beck’s theory?

A mental framework used to interpret new situations.

What is a negative self-schema?

A schema centered on negative beliefs about oneself.

How do negative self-schemas affect perception?

They cause individuals to interpret information in a biased, negative way.

Name three cognitive biases Beck identified in depression.

1. Magnification 2. Minimization 3. Personalization.

What is polarized thinking (dichotomous thinking)?

Seeing things in black-and-white terms.

How do cognitive biases maintain depression?

They distort reality, confirm negative schemas, and prevent adaptive coping.

What did Boury et al. (2001) find?

Depressed patients were more likely to misinterpret information negatively.

What did Evans (2005) study show?

Pregnant women with negative self-beliefs were more likely to develop depression later.

What did Joseph Cohen et al. (2019) demonstrate?

Cognitive vulnerability in adolescents predicted later depression.

What did Dohr et al. (1983) find?

Negative self-beliefs during depressive episodes disappeared after recovery.

How does Lewinsohn et al. (2001) offer a middle ground?

Found that negative thinking in non-depressed individuals predicted depression after negative life events.

What does the ABC model stand for?

A = Activating Event, B = Beliefs, C = Consequences.

According to Ellis, what causes depression?

Not the activating event itself, but the irrational beliefs about the event.

What is musturbation?

Irrational belief that one must be perfect.

What is utopianism?

Belief that life should always be fair and just.

What are I-can’t-stand-it-itis beliefs?

Belief that not getting what one wants is unbearable.

How do these beliefs lead to depression?

They set unrealistic standards, guaranteeing disappointment.

What is a major strength of cognitive explanations?

They have led to effective treatments like CBT.

What is a reductionist critique of Beck’s theory?

It reduces depression to cognitive dysfunction.

What is a methodological weakness in cognitive research?

Heavy reliance on self-report measures.

What limitation does Ellis’s model have regarding depression subtypes?

It mainly explains reactive depression.

How do cognitive explanations integrate with other perspectives?

They are often combined in biopsychosocial models.

How does CBT apply Beck’s theory?

It helps clients identify and challenge negative automatic thoughts.

How does REBT apply Ellis’s model?

It disputes irrational beliefs and encourages rational thinking.

What is the key debate regarding negative thinking in depression?

Whether it is a causal factor or merely a symptom of the disorder.

What evidence supports the causal role of cognition?

Longitudinal studies showing negative thinking predicts later depression.

What evidence supports the consequence view?

Studies showing negative thoughts diminish after recovery.