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what is causality/ aetiology
The study of factors, mechanisms and relationships between factors and mechanisms that cause mental distress
what is causal attribution
every-day, common-sense explanations of behaviour and its consequences
How is clinical psychology predicted
Sufficient causes
The outcome (Y) should always occur when causal factor is present
Currently none for mental distress
e.g., depression does not always occur after abuse, low serotonin, poverty, inequality, bullying etc.
Necessary causes
Y never occurs without the prior occurrence of X. Currently none for mental distress
Insufficient causes
Y occurs only after X occurs alongside another variable (Z). E.g., a person might develop schizophrenia (Y) only when they carry a genetic susceptibility (Z) and are exposed to a life stressor (X)
Difficulties with causality in mental distress
cross sectional studies- not prospective
impossible to include all influences due to time periods, different places & interactions
practical & ethical limitations in manipulating influences (e.g., ethnicity & trauma)
sensitive~ sampling bias
often not aware of/ cannot articulate all factors
unconscious biases (e.g., norms & values)
measurement- lack of validity on diagnostic categories, descriptive labels, can have different forms
3 broad approaches to study causality
deductive approach
inductive approach
epidemiological approach
Deductive approach
Tests a theory of causality using pre-determined values (surveys, experiments)
Inductive approach
Explores experiences, and links them to causal theories OR devise new causal theories (case studies, interviews, focus groups)
Epidemiological approach
Studies determinants and distribution of health-related topics.
Outline a survey method
Ask participants directly about the occurrences of variables associated with distress. (Clinical interviews, self-report questionnaires)
Participants can be sampled via quasi-random sampling. e.g., every 20th person on electoral register.
Uses a predefined range of variables of interest.
Advantages of survey methods
Useful if large random samples are used together with valid and reliable clinical instruments
Explores real variation in influences and mental distress
Can be used longitudinally
Disadvantages of survey methods
Data depends on the questions being asked and the preconceptions of the researcher
Depends on what participants are able and willing to tell the researchers
Some people with relevant mental health experiences might be excluded if quasi-random sampling is used
Outline experimental method
Manipulate a variable (X) to explore its effect on another variable (Y)
Random sampling of participants
The sample is then divided into an experimental and a control group
Differences are compared between the groups in a set of relevant measures.
e.g., RCTs
Advantages of experiments
Can provide the strongest inference of causality
High internal validity since they provide a controlled environment
Disadvantages of experiments
Cannot be generalised to the entire population (small sample)
Does not test hypotheses
Can be difficult to relate back to quantitative findings (specific)
Epidemiogical studies
Medical approach
Study the determinants and distribution of health-related topics.
Frequently uses clinical information gathered by doctors and other professionals
Studies how frequently diseases occur in different populations
Link variations in the prevalence of diseases to other variables
e.g., SES, lifestyle choices, employment history…
Advantages of epidemiological studies:
Often provides the most comprehensive picture of associations between demographic characteristics, lifestyle variables, and distress
Can access in-patient, clinic and hospital populations (and community samples)
Can be more effective than survey methods due to its access to clinical information
Disadvantages of epidemiological studies
Data is based on diagnostic categories, which are argued to lack validity
Prone to pre-existing biases that are difficult to measure
relational factors
families
early experiences
trauma & abuse
biological factors
neurotransmitters
brain structure
genetics
social factors
inequalities/poverty
gender/sexual orientation
ethnicity/disability
Models
Neurodevelopmental models
Trauma models
Traumagenic neurodevelopmental models
Biopsychosocial models
What is the biomedical model (BMM)
Assumes that individual differences in biological processes
E.g. neurotransmitters, genes, brain structure and functioning cause mental distress.
Serotonin hypothesis- depression caused by low levels of serotonin= low mood
Dopamine levels and schizophrenia
Temporal lobe and schizophrenia
Frontal lobe and depression
There is no meaningful distinction between mental and physical diseases
Mental distress can be treated with biological treatments
Erritzoe et al study (2023)
Brain imaging comparing 17 ppts with depression to 20 healthy controls.
Gave amphetamine to stimulate serotonin release
Measured how much serotonin was binding to receptors in the brain using radio-active tracing.
Participants diagnosed with depression had a lower level of serotonin compared to controls
Suggests reduced neurotransmission of serotonin in people with depression
Early 20th century methods
Penicillin
Electro-convulsive therapy (ECT) to stimulate activity in regions of the brain.
Lobotomies as a treatment approach, e.g. for depression and schizophrenia
Psychopharmological revolution (1950s-1960s)
Medication to reduce mental distress
Introduction of the chemical imbalance theory of depression.
Publication of DSM-III in 1980 introducing diagnostic criteria for mental distress.
Marketing of biomedical advances and growing collaborations with the pharmacological industry.
Growing ties between patient advocacy groups, APA, and National Institutes.
Criticisms of BMM
No clear evidence for the chemical imbalance theory when pooling results together
Moncrieff et al., 2022; Read & Moncrieff, 2022
SSRI efficacy does not prove that depression is caused by reduced levels of serotonin
Lacasse & Leo, 2005.
Biological differences might result from medication or mental distress
Causal relationship is the other way around
(e.g., Moncrieff et al., 2022), which is often not controlled for in research)
Schmall et al (2015)
Looked at hippocampus
Depression associated with smaller hippocampus
Hippocampi volume positively associated with number of depressive episodes
Criticism of Schmall et al
Criticisms
Promotion, research funding, and selective reporting (Deacon, 2013; Ioannidis, 2008).
Biomedical beliefs might increase stigma (Clement et al., 2010; Schomerus et al., 2012)
Validity of diagnostic categories (e.g., DSM) – can we even identify biomarkers for such heterogeneous experiences?
E.g., depression can be diagnosed with 227 different symptom combinations
Reductionist
Is it realistic to ignore non-biological factors that might cause distress?
Does it map onto the causal beliefs that people have about their own experiences of mental distress?
Read et al (2015)
Large sample of > 1800 ppts in New Zealand who were prescribed anti-depressants
Were asked their causal beliefs- Diverse range of causal beliefs, e.g. chemical imbalance, stress, relationship problems, childhood trauma
Those with biomedical causal beliefs thought of anti-depressants as more effective
But – sampling bias
Kemp et al (2014)
Experiment in ppts with recurrent depression:
Ppts were either told that they had low (condition 1) or normal (condition 2) serotonin levels
Measured expectations about prognosis/recovery
Ppts in the ‘low serotonin’ condition were more pessimistic about their recovery
Larkings et al (2017)
Thematic analysis of semi-structured interviews with 23 service users
Participants felt that causal beliefs were important, frequently thought about them
But, were rarely addressed in treatment
Could increase insight, symptom management, and reduce self-blame
Congruence with clinician is key for therapeutic alliance and recovery process