1
, Course objectives
● You can explain the most important theoretical and scientific concepts in the field of
prevention of mental health problems.
● You can demonstrate a basic understanding of methods to identify who is at risk for
developing mental health problems.
● You can discuss the relevance of different risk and protective factors for mental health
problems.
● You can describe relevant prevention programs for different mental health problems and the
evidence for its effectiveness.
● You can conduct a systematic and critical review of the scientific literature in the field of
mental health prevention programs and report on it.
● You can integrate gained knowledge on mental health prevention to make
recommendations for further research and practice.
Lecture 1: Introduction
The World Health Organization (WHO) monitors the prevalence + incidence of disorders worldwide
including mental disorders.
Epidemiological transition:
- Worldwide shift from communicable (infectious disease) → Non-Communicable disease
(NCD)
- Increase in life expectancy: Premature mortality → Disease burden: years of lost life due to
premature mortality or years lived with disability
Disease burden
Expressed in DALY’s: Daily Adjusted Life Years
- This is the amount of ‘health loss’ (caused by illness, disability or early death)
- 1 DALY is 1 year of healthy life lost
- DALY = YLL (years life lost) + YLD (years lost due to disability)
- YLD are based on generic measures of Quality of Life (QoL) and most important for the
burden of mental health disorders.
Global burden of disease
- 16% affected by mental health disorders (point prevalence)
- 7% of total disease burden (DALY’s → so incl. mortality) although this is an underestimation:
- People with personality disorders are not included
- Indirect contributions of mental health disorders to mortality
- Suicide and self-harm are grouped under injuries
- Overlap with other (neurological) disorders
- People with chronic pain disorders are not included
- ⅕ of all quality of life lost (YLD → so excl. mortality)
- Worldwide depression is ranked 2nd after HIV/AIDS
- High prevalence mental disorders: Anxiety, Depression, Addiction, etc., → account for ⅔ of
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, all DALY’s
- Low prevalence mental disorders: Bipolar disease, schizophrenia, Eating disorders, Autism,
etc. → account for ⅓ of all DALY’s.
Worldwide variations
- Higher mental health (MH) burden in wealthier countries and countries with high income
inequality
- In Low and Middle Income Countries (LMIC): poverty was related to more MH burden
- BUT empirical evidence from LMIC is scarce and based on population surveys
- treatments in LMIC are still lacking so the impact is more devastating
Prevention vs. treatment
Averted YLD with treatment:
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Treatment doesn’t avert disease burden 100%. There’s an opportunity for prevention!
- 11-27% reduction of disease burden possible by prevention
- Prevention offers new and cheaper options
Classification of prevention
Traditional medicine distinguishes between primary (before onset), secondary (curing) and tertiary
(focusing on QoL) care. Mental Health distinguishes between:
- Universal prevention: targeting a population (e.g. fostering resilience and reducing risk)
- Selective: target subgroups that are at risk (who have not yet symptoms)
- Indicated: target people in the early stages who experiences symptoms (therefore they use
screening for symptoms and behaviours).
The mental health intervention spectrum:
Health promotion vs. prevention
- Health promotion: promotes
positive health by increasing well
being, competence, resilience &
creating supportive living
conditions and environments
- Health prevention: reduction of
incidence, prevalence, recurrence
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, of disorder
Problems with classification
- Indicated prevention and early treatment are hard to distinguish
- Selective and indicated prevention are hard to distinguish
- Prevention and continuing care (see figure ‘maintenance’)
- Preventing comorbid disorders?
- Preventing relapse?
- Prevention focused on relatives!
Choosing an intervention
- Choosing between e.g. a ‘light’ universal prevention method, reaching many people, or
reach a selected population with a more intensive prevention method?
- Cost-effectiveness
- Problems that can arise:
- You don’t know if the disorder will occur and it’s often unknown who will develop a
disorder. Therefore efforts may be a waste of time for some people
- People can lack motivation
- It can be stigmatizing (in this case a prevention method could do more harm than
good).
Who’s at risk?
Diathesis-stress model
- Diathesis: predisposition or vulnerability to a
disorder
- Stress: the occurrence of some severe
environmental or life event
- They’re both necessary to develop a disorder
Risk factors: factors that interact to have direct or indirect effects on the development of
psychopathology. (Causality is difficult to determine). Measurable characteristic that precedes the
onset of a disorder.
- stressful environmental or life events
- temperamental and personality traits
- neurobiological factors
- cognitive processes and biases
- genetic make-up
Difference in generic risk-factors (predicts onset of any psychological disorder e.g. poverty,
upbringing, abuse) and disease specific risk-factors (e.g. negative thinking style for depression).
Protective factors: Protect against developing psychopathology, like: feelings of control; good
interpersonal relationships; social support; high self-esteem; and good health. These can be the
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,focus of preventive interventions. Network analysis can help understand risk and protective factors
in relation to disorder onset (see lecture suicide).
Programmatic approach
- Micro-level: individual
- Meso-level: community
- Macro-level: societal (e.g. not smoking inside bars)
Preventive methods
Can differ in format and setting.
- Policy: e.g. ban on smoking inside
Formats:
- psycho-education
- support and contact groups (can include psycho-education, contact with fellow sufferers,
exchanging experiences and emotions, teach coping skills)
- (guided) self-help (advantages: accessible, cheap, 24-7 availability, less stigmatizing).
- courses or training programs
- skills improvement
Settings:
- Mass media campaigns
- School-interventions (Main topics: school dropout, substance use, risky sexual behaviour,
delinquency, suicide, bullying).
- Higher-education (e.g. ‘Caring Universities’)
- work-place (Main topics: stress, depression, social skills, vitality, time-management)
- Hospital (Practical problems, Family/social problems, emotional problems, spiritual
problems)
- Community
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, Lecture 2: Prevention of PTSD
Types of PTSD prevention:
- Preparing on predictable stressful events
- Debriefing and crisis counselling
- Early PTSD risk screening
- Early treatment for trauma victims with acute (symptoms of) PTSD or acute stress disorder
(ASD)
- Innovations: e.g. pharmacotherapy, Tetris
DSM-5 Criteria PTSD
● Criterion A: stressor (one required): Direct exposure / Witnessing the trauma / Learning that
a relative or close friend was exposed to a trauma /Indirect exposure to aversive details of
the trauma, usually in the course of professional duties, e.g. first responders, medics (this is
different than seeing a video clip for one time on the internet).
● Criterion B: intrusion symptoms (one required). The traumatic event is persistently re-
experienced in the following way(s): Unwanted upsetting memories / Nightmares
/Flashbacks / Emotional distress after exposure to traumatic reminders / Physical reactivity
after exposure to traumatic reminders
● Criterion C: avoidance (one required). Avoidance of trauma-related stimuli after the trauma,
in the following way(s): Trauma-related thoughts or feelings/ Trauma-related external
reminders
● Criterion D: negative alterations in cognitions and mood (two required): Negative thoughts
or feelings that began or worsened after the trauma, in the following way(s): Inability to
recall key features of the trauma / Overly negative thoughts and assumptions about oneself
or the world / Exaggerated blame of self or others for causing the trauma /Negative affect /
Decreased interest in activities / Feeling isolated / Difficulty experiencing positive affect
● Criterion E: alterations in arousal and reactivity. Trauma-related arousal and reactivity that
began or worsened after the trauma, in the following way(s): Irritability or aggression / Risky
or destructive behavior / Hypervigilance / Heightened startle reaction / Difficulty
concentrating / Difficulty sleeping
4 trajectories of PTSD: Resilient, recovering, chronic, delayed onset:
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,Risk factors
Neuroendocrine response
Working mechanism theory: Dysregulated HPA function is a vulnerability factor in PTSD → Lower
cortisol levels lead to failure to trigger the negative feedback loop. This prolongs the adrenergic
response, and may exacerbate consolidation of the traumatic memory.
A meta-analysis found no overall predictive effect of early cortisol levels on PTSD symptoms, but
they found a predictive effect of cortisol, age dependent.
Fear conditioning
PTSD perceived as disorder of impaired fear extinction. Extinction involves inhibitory fear learning:
Conditioned stimulus (CS) has 2 meanings CS-UCS (excitatory) and CS-no UCS (inhibitory). Reduced
inhibitory fear learning at 2 months after military deployment predicted PTSD symptoms at 9
months. Effect remained after controlling for trauma history and PTSD symptoms at 2 months.
Systematic review and meta-analysis on pharmacotherapy to prevent PTSD
- Administered less than a month after trauma
- No significant difference between beta-blockers and hydrocortisone
- No firm evidence for effectiveness of early pharmacotherapy in prevention of PTSD or ASD
(acute stress disorder)
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, - hydrocortisone reduced risk of development of PTSD
- Hydrocortisone promising option for PTSD prevention in crisis situation
- But side effects; and more drop-outs in pharmacotherapy, so people might not want it; and
not sure how it affects memory yet (which could be troubling in law-suits).
Future directions
- Larger rigorous studies on hydrocortisone and other promising options (e.g. oxytocin,
morphine) necessary.
Memory consolidation
● it takes 6 hours to consolidate trauma from working memory into long-term memory.
● Intervention: Tetris:
○ Study: healthy people who played tetris for 30 minutes vs. no computer game, after
watching a trauma film. Tetris player had fewer intrusions during week.
○ Study: emergency room patients; 20min tetris vs. attention-placebo control.
Significant effect for intrusions at one week, not for PTSD symptoms at one month.
○ Study: people exposed to emergency c-section: 10 minutes of Tetris or no game
control. Significant effects for intrusions at one week, not for PTSD symptoms.
○ Working mechanism: disrupts memory consolidation?
● Imagery rescripting:
○ Content: Participants imagining different responses to and outcomes of the original
event and its aftermath
○ Working mechanism: Degrades the valence and meaning of the original event
○ Outcome: Reduces intrusions after trauma film in health participants.
● → Other study with healthy participants showed that Tetris was more effective than imagery
rescripting or control group. Tetris group showed fewer intrusions during week.
Current status field of PTSD prevention: Exciting pharmacological and cognitive options, in need of
larger effectiveness trials.
2.1 Qi W, Gevonden M, Shalev A. (2016).
Prevention of Post-Traumatic Stress Disorder After Trauma: Current Evidence and Future Directions.
Curr Psychiatry Rep, 18(2), 20.
Empirical findings and theoretical models have outlined specific risk factors and pathogenic
processes leading to PTSD. Research had shown that theory-driven approaches as CBT and stress
hormone-targeted pharmacological interventions are efficacious in selected samples of survivors.
The clinical features of PTSD are event-related symptoms (intrusive recall of aspects of the event,
avoidance of reminders and hypervigilance) along with dysphoria, hyperarousal or anhedonia. PTSD
may persist for years and decades in (some) trauma-exposed survivors. PTSD can be chronic if not
treated well. Chronic PTSD is associated with poor physical health, inferior well-being and
unemployment, and is often co-morbid with mood-, anxiety-, and substance use disorders.
PTSD offers unique opportunities for early detection and prevention:
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, - It has a distinct stressor and clear onset point (unlike other MH disorders)
- Early symptoms develop within days of trauma exposure
- Organized professional response: many trauma-exposed individuals are brought to the
attention of emergency care services and helpers
The disorder’s prevalence in the last four decades is stable. Several possibilities of this are that
efficiënt interventions have not been implemented on a large scale; risk detection is imperfect;
service delivery can be difficult.
Theoretical Models and Intervention Targets
Individual risk predictors include
- pre-exposure ‘vulnerability’ factors (in lecture
called pretrauma factors): genetic
vulnerability, female sexe, low age,
intelligence ( a higher IQ is a protective
factor), low SES, prior trauma, prior
psychiatric symptoms
- peri-trauma factors = around traumatic
event: trauma intensity and type (e.g.
intentional vs. unintentional); physiological arousal; perceived threat; negative
interpretation of event (e.g. the thought you were dying); physiological arousal; anger and
shame; dissociation during event (higher risk, probably a more heavy reaction to stress).
- Posttrauma reactions = reactions directly related to the event and post-exposure
adversities: Social support (protective); coping; negative interpretation of consequences of
event; new life events (e.g. unemployment because of event).
This knowledge has not yet been translated into individual risk prediction. One shortcoming of
research is the statistical modeling that doesn't account for heterogeneities: each exposed individual
brings his own range of factors to the event.
See figure in article: this presents the main theoretical models of PTSD pathogenesis, linking each
model with specific interventions. Timing of an intervention is crucial, e.g. memories may
consolidate within hours of trauma or during the first nights sleep.
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, Theory Driven interventions
Theory informed vs. non-theory informed
Overview of Preventive interventions
Psychological or behavioral interventions
● Psychological debriefing
○ Previously widely used
○ Aim: preventing long-term post-traumatic symptoms by promoting quick emotional
processing of traumatic events shortly after trauma exposure
○ Offered to: people being exposed, without prior diagnoses or evaluation. (Sound like
selective prevention).
○ Content: education about trauma exposure, sharing experiences, preparation for
future encounters.
○ Not recommended: no evidence of beneficial effects, and may even be harmful! It
disturbs recovery in highly aroused trauma survivors.
● Trauma-focused CBT: can involve different strategies with distinct aims
○ Exposure-based CBT:
■ Aim: achieve and maintain fear extinction
■ Working mechanism: through repeated exposure to trauma-related stimuli
in a safe context, it will provide a sense of control over reactions and reduce
avoidance.
■ Moderately positive results
○ Cognitive-based CBT:
■ Content/Working mechanism: challenges the patiënt’s belief about the
meaning and current implication of the trauma.
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