Depression & Anxiety – Clinical Psychology Week 2
DEPRESSION
WHAT IS DEPRESSION? — LIVED EXPERIENCE
"How weary, stale, flat and unprofitable seem to me all the uses of this "All sense of hope vanished… my brain had become less an organ of
world" — Shakespeare's Hamlet thought than an instrument registering, minute by minute, varying degrees of
"Each day I awoke deeply tired, a feeling as foreign to my natural self as an anxiety it was no longer possible to keep at bay"
being bored and indifferent to life"
DSM-5 DEPRESSIVE DISORDERS OVERVIEW & NOSOLOGY NOTES
DSM-5 depressive disorders include: Disruptive Mood Dysregulation Culture & Symptoms — Haroz et al. (2017):
Disorder · Major Depressive Disorder · Persistent Depressive Disorder
DSM-5 has limitations around symptomology — culturally biased, based on
(Dysthymia) · others
experiences that reflect Western contexts. Depression manifests differently
Nosology note: DSM-5 uses categorical diagnoses — symptoms grouped in other cultures. Haroz et al. found depressive experiences may include
into discrete categories. But many features of MDD (low mood, anhedonia, culturally salient symptoms such as bodily pain, social
fatigue) exist on a continuum in the population. This is a limitation: people isolation/loneliness, crying, anger, headaches, thinking too much,
near the diagnostic threshold may be classified very differently despite worry.
similar presentations. Clarification: DSM symptoms are not useless; clinicians should be cautious
about assuming Western symptom presentations are universal. The cultural
Critical distinction: Diagnosis and aetiology should be separated. DSM- context of the patient matters.
5 describes which symptoms count as MDD, but it does not fully explain why
those symptoms occur. Clinicians should not assume that meeting DSM
criteria answers questions about cause.
DSM-5 MAJOR DEPRESSIVE DISORDER CRITERIA
Five or more symptoms in a two-week period, representing a change Functioning impairment criteria: Symptoms cause clinically significant
from previous functioning. At least one must be depressed mood OR distress or impairment in social, occupational, or other important areas of
anhedonia. functioning. Distinguishes MDD from transient distress.
Core symptoms:
Depressed mood most of the day, nearly every day Nosological/evaluation point: The threshold approach helps distinguish
MDD from transient distress, but it can mean that two patients with very
Markedly diminished interest or pleasure (anhedonia)
different symptom profiles share the same diagnosis. MDD is highly
Significant weight loss or gain / appetite change
heterogeneous — the same label can describe very different presentations.
Insomnia or hypersomnia
Psychomotor agitation or retardation Who gets depression: 5.7% of world's adult population · female:male ratio
Fatigue or loss of energy 1.5:1 · ranked largest contributor to non-fatal health loss (7.5% of all YLDs) ·
Feelings of worthlessness and/or guilt most prevalent in low- and middle-income countries · comorbid with anxiety
Diminished ability to concentrate or indecisiveness (WHO, 2025)
Recurrent thoughts of death or suicidal ideation
, Depression & Anxiety – Clinical Psychology Week 2
CONSEQUENCES & BIOLOGICAL ASPECTS OF MAJOR DEPRESSION
Consequences of Major Depression: The Monoamine Hypothesis — biological perspective:
Cognitive functioning — can become very serious; cog functioning can Proposes that depression results from depletion in the levels of monoamine
be indistinguishable from that of dementia neurotransmitters — particularly serotonin, noradrenaline and/or
Occupational functioning — impaired work performance, absenteeism, dopamine.
job loss Antidepressants (SSRIs, SNRIs, TCAs) work by increasing synaptic
Social relationships — withdrawal, conflict, relationship breakdown availability of these monoamines — supporting the hypothesis clinically.
Suicide — significant risk; depression is a major risk factor Evidence for: antidepressants targeting these systems show clinical benefit;
depressed patients show altered monoamine levels and receptor function
Biological aspects — evidence base:
Symptoms (appetite, sleep, fatigue) reflect biological dysregulation —
people somatise the experience (psychological distress
experienced/communicated through bodily symptoms)
Depression runs in families — suggests a genetic link
Brain imaging (PET, fMRI, MRI) — functional and structural changes; also
shown post-mortem in those with MDD
Key evaluation question: Do changes in the brain precede symptoms?
Brain differences may be causes, consequences, correlates or
vulnerability markers
Changes in neurotransmitter and hormone levels
Success of biological treatments (antidepressants, ECT)
No biological markers for mental health disorders — clinicians focus on
symptoms and criteria
MONOAMINE HYPOTHESIS — FIGURE & EVALUATION
Cumulativeremissionrateby
STAR*Dtreatmentlevel
80
70-
Cumulativeremission
60—
50⼀
40—
30-
20—
10-
0 1 2 3 4
Treatmentstep
Pathophysiologic basis of depression — monoamine depletion figure (image1)
DEPRESSION
WHAT IS DEPRESSION? — LIVED EXPERIENCE
"How weary, stale, flat and unprofitable seem to me all the uses of this "All sense of hope vanished… my brain had become less an organ of
world" — Shakespeare's Hamlet thought than an instrument registering, minute by minute, varying degrees of
"Each day I awoke deeply tired, a feeling as foreign to my natural self as an anxiety it was no longer possible to keep at bay"
being bored and indifferent to life"
DSM-5 DEPRESSIVE DISORDERS OVERVIEW & NOSOLOGY NOTES
DSM-5 depressive disorders include: Disruptive Mood Dysregulation Culture & Symptoms — Haroz et al. (2017):
Disorder · Major Depressive Disorder · Persistent Depressive Disorder
DSM-5 has limitations around symptomology — culturally biased, based on
(Dysthymia) · others
experiences that reflect Western contexts. Depression manifests differently
Nosology note: DSM-5 uses categorical diagnoses — symptoms grouped in other cultures. Haroz et al. found depressive experiences may include
into discrete categories. But many features of MDD (low mood, anhedonia, culturally salient symptoms such as bodily pain, social
fatigue) exist on a continuum in the population. This is a limitation: people isolation/loneliness, crying, anger, headaches, thinking too much,
near the diagnostic threshold may be classified very differently despite worry.
similar presentations. Clarification: DSM symptoms are not useless; clinicians should be cautious
about assuming Western symptom presentations are universal. The cultural
Critical distinction: Diagnosis and aetiology should be separated. DSM- context of the patient matters.
5 describes which symptoms count as MDD, but it does not fully explain why
those symptoms occur. Clinicians should not assume that meeting DSM
criteria answers questions about cause.
DSM-5 MAJOR DEPRESSIVE DISORDER CRITERIA
Five or more symptoms in a two-week period, representing a change Functioning impairment criteria: Symptoms cause clinically significant
from previous functioning. At least one must be depressed mood OR distress or impairment in social, occupational, or other important areas of
anhedonia. functioning. Distinguishes MDD from transient distress.
Core symptoms:
Depressed mood most of the day, nearly every day Nosological/evaluation point: The threshold approach helps distinguish
MDD from transient distress, but it can mean that two patients with very
Markedly diminished interest or pleasure (anhedonia)
different symptom profiles share the same diagnosis. MDD is highly
Significant weight loss or gain / appetite change
heterogeneous — the same label can describe very different presentations.
Insomnia or hypersomnia
Psychomotor agitation or retardation Who gets depression: 5.7% of world's adult population · female:male ratio
Fatigue or loss of energy 1.5:1 · ranked largest contributor to non-fatal health loss (7.5% of all YLDs) ·
Feelings of worthlessness and/or guilt most prevalent in low- and middle-income countries · comorbid with anxiety
Diminished ability to concentrate or indecisiveness (WHO, 2025)
Recurrent thoughts of death or suicidal ideation
, Depression & Anxiety – Clinical Psychology Week 2
CONSEQUENCES & BIOLOGICAL ASPECTS OF MAJOR DEPRESSION
Consequences of Major Depression: The Monoamine Hypothesis — biological perspective:
Cognitive functioning — can become very serious; cog functioning can Proposes that depression results from depletion in the levels of monoamine
be indistinguishable from that of dementia neurotransmitters — particularly serotonin, noradrenaline and/or
Occupational functioning — impaired work performance, absenteeism, dopamine.
job loss Antidepressants (SSRIs, SNRIs, TCAs) work by increasing synaptic
Social relationships — withdrawal, conflict, relationship breakdown availability of these monoamines — supporting the hypothesis clinically.
Suicide — significant risk; depression is a major risk factor Evidence for: antidepressants targeting these systems show clinical benefit;
depressed patients show altered monoamine levels and receptor function
Biological aspects — evidence base:
Symptoms (appetite, sleep, fatigue) reflect biological dysregulation —
people somatise the experience (psychological distress
experienced/communicated through bodily symptoms)
Depression runs in families — suggests a genetic link
Brain imaging (PET, fMRI, MRI) — functional and structural changes; also
shown post-mortem in those with MDD
Key evaluation question: Do changes in the brain precede symptoms?
Brain differences may be causes, consequences, correlates or
vulnerability markers
Changes in neurotransmitter and hormone levels
Success of biological treatments (antidepressants, ECT)
No biological markers for mental health disorders — clinicians focus on
symptoms and criteria
MONOAMINE HYPOTHESIS — FIGURE & EVALUATION
Cumulativeremissionrateby
STAR*Dtreatmentlevel
80
70-
Cumulativeremission
60—
50⼀
40—
30-
20—
10-
0 1 2 3 4
Treatmentstep
Pathophysiologic basis of depression — monoamine depletion figure (image1)
