PY0547_Week 11_Depression_ES_forBB
Introduction
Course: PYO547 Psychobiology I
Instructor: Dr. Ellen Smith
Focus: Biological basis of Depression
Sensitive Topics
Discussion of sensitive topics, including:
Low mood
Suicide
Students feeling unsettled should opt for alternative activities and seek support if needed.
Definition of Depression
Long-lasting negative affect (negative hedonic feelings)
Associated feelings: powerlessness, lack of motivation, inability to influence events (Beck, 1967)
Prevalence of Depression
Affects over 280 million people worldwide (WHO, 2023)
Leading cause of disability (WHO, 2020)
Gender disparity: Women are twice as likely to suffer from depression compared to men (Girguis & Yang, 2015)
Severe cases can lead to suicide, with over 700,000 deaths annually. It is the third leading cause of death in individuals aged 15-29 (WHO, 2024).
Lecture Overview
Topics to cover:
Terms & Symptoms of Depression
Causes (Biological, Environmental & Psychological Models)
Treatments (Pharmacological & Non-pharmacological)
Optional learning activities
Terms and Symptoms
Types of Mood Disorders
Unipolar Depression: Prolonged sadness and despondency.
Bipolar Depression: Alternating periods of depression and mania.
Dysthymia (Persistent Depressive Disorder): Milder, long-lasting version of major depression.
Cyclothymia: Milder, long-lasting bipolar disorder version.
Symptoms of Major Depressive Disorder (MDD)
Emotional Symptoms
Sadness, tearfulness, misery
Low self-esteem, helplessness
Cognitive Symptoms
Rumination, perception issues, attentional difficulties
Memory problems
Motivational Symptoms
Energy loss, decreased goal-oriented behavior
Physical Symptoms
Sleep disturbance, appetite loss, aches and pains
Loss of libido, weight changes
Biological Models of Depression
Monoamine Hypothesis
Proposed by Joseph Schildkraut, based on initial findings regarding neurotransmitters.
Key Neurotransmitters
Monoamines include serotonin, norepinephrine, and dopamine.
Evidence:
Anti-hypertension drug (reserpine) depletion leads to depression.
Anti-tuberculosis drug (iproniazid) boosts monoamine levels, alleviating depression.
This hypothesis spawned the first antidepressants and is sometimes called the neurotransmission hypothesis.
Mechanism of Action (Normal vs. Depressed)
Non-depressed State
Efficient synthesis and transport of monoamines.
Monoamines bind effectively to post-synaptic receptors for signal transmission.
Depressed State
Inefficient synthesis and re-absorption of monoamines leading to insufficient levels for binding at post-synaptic neurons.
Anti-depressant Treatments
Aim to increase monoamine availability in the synapse through:
Blocking reabsorption (SSRIs)
Inhibiting monoamine-degrading enzymes (e.g., Monoamine Oxidase inhibitors)
Critiques of the Monoamine Hypothesis
Cannot fully explain treatment-resistant depression, as up to 30% do not respond to standard treatment.
Latency period (2-6 weeks) for response is unexplained.
The hypothesis is considered overly simplistic.
Neuroplasticity Theory
Focuses on reduced neuroplasticity leading to neuron loss and lower neurotrophin synthesis (e.g., BDNF).
Neuroplasticity refers to the brain's ability to reorganize itself and form new neural connections.
Evidence Support
Decreased neuroplasticity observed in hippocampus and PFC of depressed patients.
Antidepressants may improve neuroplasticity and increase concentrations of neurotrophic factors.
Stress and Depression
Major depressive episodes correlate with an increase in stressful life events (Hammen, 2005).
The Hypothalamus-Pituitary-Adrenal-Axis (HPA) response is crucial in understanding the biological mechanisms.
Chronic Stress Effects
Prolonged elevation of cortisol from chronic stress is neurotoxic, affecting hippocampal neurons and functionality.
A vicious cycle occurs with continued stress exacerbating structural and functional deficits.
Neurotransmitter Interaction
Chronic stress dysregulates stress hormone systems, altering neurotransmitter balances and potentially leading to depression.
Gene-Environment Models of Depression
Twin Studies
Bierut et al. (1999): Examined monozygotic and dizygotic twins for major depression correlation, highlighting genetic and environmental influences.
Gene-Environment Interactions
Caspi et al. (2003): Identified that individuals with short serotonin transporter genes have increased depression risk under stress, contrasting with those with variant responses.
Stressful events interplay with genetic predispositions to modulate depression risk.
Resilience Factor
Wingo et al. (2010) indicates that resilience can mitigate depression severity related to childhood trauma.
Psychological & Environmental Factors
Psychological Processing Biases
Depressed individuals tend to focus on negative information, affecting their cognitive processing and emotional responses.
Environmental Triggers
Factors such as single parenthood and unemployment increase depression risk. Odds ratios help assess these associations with outcomes.
Treatments for Depression
Pharmacological Treatments
SSRIs enhance monoamine availability by blocking reabsorption or inhibiting breakdown enzymes.
Non-Pharmacological Treatments
Comparatively effective outcomes between drugs, cognitive behavioral therapy (CBT), or their combination (Amik et al., 2015).
Psychological Therapies Include:
Cognitive Behavioral Therapy
Interpersonal therapy
Other therapeutic approaches
Conclusion
Covered:
Types and symptoms of depression
Biological, environmental, social, and psychological explanations
Treatments (both pharmacological and non-pharmacological)
Emphasis on mental health care alongside physical health.
Resources and Support Links
Various links for mental health support, counseling, workshops, and self-help resources.
Essential Reading
A selection of key readings and further resources regarding the biological and environmental underpinnings of depression.