Lecture 1: Introduction to Psychopathology

 The final exam is in person. You must LEARN this content.

 Essay topic: “DSM anxiety disorders are not genuine states of mental ill-health. Due
28/4. Does everybody have it? You need to be concerned with future directions, ways
to resolve the scholarly work you cover.
 Lectures week 1-5 start at 9:30, and then after they will start at 9:00.
 What is mental health? “Mental health is a state of well-being in which the individual
realises his or her own abilities, can cope with normal stresses of life, and is able to
make a contribution to his or her community.” – World Health Organisation, 2007.
Note that mental health is not just the absence of psychological problems.
 What is mental illness? “A clinically diagnosable disorder that significantly interferes
with an individual’s cognitive, emotional or social abilities.” – Department of Health
and Aged Care. Note how this conception is very holistic.
 National study of mental health and wellbeing:
o Prevalence:

o Lifespan:
 o Anxiety disorders:

 Dunedin cohort study: Very famous study following a large group from when they
were born into middle life, taking into account lots of factors. They found that by
middle age, only 14% of that cohort had not met criteria for a diagnosable mental
disorder. 86% had met diagnostic criteria for at least on psychological disorder by
mid-life. Many had met criteria for more than one. When we’re talking about
disorders, we are talking about something that is very likely to affect us in our
lifetime.
 Psychological health and illness: These are the kinds of questions we are dealing with
over the semester
o What is normal or helathy? Being like the majority? Autonomous functioning?
Accurate reality perception? Regulated moods? Adequate interpersonal
relationships?
o How does one distinguish between mental health and ill-health? What criteria
do we bring to bear in making this judgement? Where can we draw the line
between health and illness? In physical health, this can be a complicated
question.
o For most clinicians, a diagnosis really embodies a decision to treat. This can
involve many different treatment methods. Context is the key to understanding
a person and whether they are mentally healthy.
o What is a “mental disorder”? The fifth edition of the Diagnostic and Statistical
Manual of Mental Disorders (the DSM-5) is used as the current authoritative
listing of mental disorders. It broadly defines mental disorder as: “clinically
significant disturbance in an individual’s cognition, emotion regulation or
behaviour…usually associated with significant distress or disability in social,
occupational or other important activities” (DSM-5).
o We still need to unpack clinical significance. We are usually talking about
more extreme forms of otherwise broad ubiquitous psychological experience.
Clinical significance is about the severity of symptoms, frequency of
symptoms, the intrusiveness of symptoms, the functional impact on the
person, the length of disturbance, and a range of other contextual factors.
o What is not a mental disorder? The DSM-5 goes on to define what does not
constitute a mental disorder: “an expectable or culturally approved response to
 a common stressor or loss, such as the death of a love one, is not a mental
disorder.”
 The subject is named the psychopathology of everyday life for a good reason. One of
the central themes of the subject is that the boundaries between mental health and ill-
health are not distinct, they’re fuzzy. This idea is raised originally in Freud’s book,
The Psychopathology of Everyday Life. He observed that the “neuroses” he would see
in everyday life would be less extreme forms of the behaviour he saw at the clinic.
Maybe the idea that diagnosis gives us (that you’re either mentally ill or you’re not)
doesn’t ring true when considering the real-world situation of mental ill-health.
 Classifying mental health issues:
o Categorical vs dimensional classification:

 Categorical: Better clinical and administrative utility – clinicians are

often required to make dichotomous decisions; Easier communication.
 Dimensional (more ecological validity): Closely model lack of sharp
boundaries between disorders and between disorders and normality;
Have greater capacity to detect change and facilitate monitoring; Can
develop treatment-relevant symptom targets not simply aiming at
resolution of the disorder (most treatments actually target symptoms,
not disorders).
o Why diagnose or classify mental health issues? Not all cultures do, and
different cultures treat what we call mental illness in different ways.
 Communication: Among clinicians, between science and practice.
 Clinical: facilitate identification of treatment, and prevention of mental
disorders, descriptive of experience, possible aetiology and prognosis.
 Research: Test treatment efficacy and understanding aetiology.
 Education: Teach psychopathology.
 Information management: Measure and pay for care
o DSM-5 Diagnostic groupings: Neurodevelopmental disorders; Schizophrenia
spectrum and other psychotic disorders; Bipolar and related disorders;
Depressive disorders; Anxiety disorders; Obsessive-compulsive and related
disorders; Trauma- and stressor-related disorders; Dissociative disorders;
Somatic symptom and related disorders; Feeding and eating disorders;
 Elimination disorders; Sleep-wake disorders; Sexual dysfunctions; Gender
dysphoria; Disruptive, impulse control and conduct disorders; Substance-
related and addictive disorders; Neurocognitive disorders; Personality
disorders; Paraphilic disorders; Other mental disorders; Medication induced
movement disorders and other adverse effects of medication; Other conditions
that may be a focus of clinical attention. (Italics are the ones covered in
subject).
 General diagnostic approach using the Diagnostic and Statistical Manual of Mental
Disorders:
o Diagnosis will be made on the basis of: clinical interview; text descriptions;
diagnostic criteria; clinician assessment
o Currently presenting symptoms and severity, e.g. depressed mood
o Rule out disorder due to general medical condition, e.g. due to hypothyroidism
o Rule out disorder due to direct effects of a substance, e.g. alcohol induced
o Establish boundary with no mental disorder: clinical significance/cultural
sanction, e.g. bereavement vs clinically significant depression
o Determine specific primary disorder(s): multiple diagnoses possible
o Add subtypes/specifiers: severity (mild, moderate, severe – with or without
psychotic features); treatment relevant (poor insight, atypical, etc.);
longitudinal course (with/without full inter-episode recovery, seasonal pattern)
o Mini example – psychotic disorders section:

 There have been several ways in which mental ill-health has been considered over
time. Some people believe experiences of mental ill-health are tied to the devil under
Catholicism, where you’ll get autistic people getting exorcisms. Below are a few
paradigms that have been used and are still somewhat in use today.
o Freudian paradigm: The unconscious has a profound influence on what we do
and how we feel in day-to-day life. Only becoming aware of unconscious
motivations (via psychoanalysis) can individuals choose less maladaptive and
more adaptive behaviour. This is the psychoanalytic tradition.
o Behavioural paradigm: Moving away from Freud (early 1900s to middle of
century), this approach focused on behaviour and cognition, that there are no
unconscious processes affecting experiences, but instead it is all about
 responses to environmental conditions. The goal of behavioural interventions
is to interrupt and/or change stimulus-response associations.
o Cognitive paradigm: Occurring in the 50s and 60s with what was called the
“cognitive revolution”. We placed primacy on thought, and the way we
appraise circumstances and situation in our life. Depending on our method of
interpretation and attribution to things in our life, this style can be

maladaptive.
o Biopsychosocial paradigm: More recently, biopsychosocial approaches to
understanding mental disorder integrates a complex range of factors:
biological (normal biology, disease processes and genetic influences);
psychosocial (thoughts, feelings and perceptions); social/environmental
(culture, ethnicity, social environment). These are dynamic, reciprocally
deterministic interactions that play out in very complex ways that we are still

trying to understand.
 Anti-psychiatry and alternative perspectives: Usually, with any psychological
disorder, we can’t point to a specific physiological process and say that it is the cause
(which we can then treat). We do not know definitively the reason for disorders.
However, with all these disorders there are many known correlates that are part of the
equation, but the interplay is very complex, and we don’t have a comprehensive
understanding, which leads to questioning of these approaches.
 o Disorders are not real. They are a creation to justify inappropriately
pathologizing, coercive and harmful treatment practices. There is some
convincing scholarly work that argues this point (Nick Haslam). Evidence for
dimensional diagnostic approach far outweighs categorical evidence.
o Maintain wealth and power of institutions including “big pharma”. This has
been particularly prominent since the development of anti-psychotic
medication.
o Enforcement of cultural norms.
o Systematically disempowering for people with lived experience. Historically,
psychiatric systems have completely deprived patients of any agency,
profoundly disempowering these people, with no say in their treatment. This
often prevented people being honest about symptoms and experiences.
o Framing psychological experience as illness is inherently harmful. Hearing
Voices will address this, and this is quite a strong argument.
o A diverse range of perspectives exist in the lived experience community
o Human rights focus.
o Mental health viewed as a “threat to public order”: “Mental health largely
became a concern when it threatened public order and governments were
particularly prominent in the management of the insane.” This led to the
development of asylums. Asylums and criminality became synonymous,
where people were put there not with the interest of the person in mind, but to
protect wider society from that threat.
 Inhumane treatments:
o Early approaches were largely focused on maintaining the safety of the public
o Little emphasis was placed on the well-being and/or recovery of the individual
with the disorder.
o Occurrences of “shell shock” during WWI showed that “normal” individuals
could succumb to “nervous” illness and created a desire for more humanistic
treatment.
o Further developments in treatment and the anti-psychiatry movement created
interest in psychosocial interventions.
o Dr Benjamin Rush’s (1745-1814) “Tranquilising Chair” is an example of such
dubious treatment. Conversely, he also argued hard for the idea that mental
illness was not demonic.
 Deinstitutionalisation:
o Stage I: New treatments led to an “open-door” policy, allowing individuals to
be treated on an outpatient basis.
o Stage II: Asylums began to close, and treatment shifted to the community.
 o Institutionalisation over time:

 Hearing voices 1: Fay Jackson and Scott Gourlay

o Fay is General Manager of Inclusion at Flourish Australia, and for the job, you
need to have had significant experience with mental health issues, it is a lived
experience position.
o Scott is a past co-chair of Flourish’s Community Advisory Council which
helps the company formulate policy and procedure. It provides a lived
experience conduit for knowledge and awareness from those people who
access Flourish services to the senior leadership team. He is also a member of
the Community Stakeholders for the Global Commission into Psychosis. He
has lived experience of psychosis.
o How do we distinguish between mental health and ill-health? You may think
it’s black and white, but the picture is far more complicated.
o Scott’s perspective on how psychosis plays out in reality: It is no black and
white, Scott lived many years unmedicated, so he was technically in a
psychotic episode the entire time, hearing voices continually, literally. He had
developed strategies to cope with these voices and function in the world
despite his level of paranoia was quite high, believing spies were monitoring
everyone, with fixed beliefs about that. Although he was experiencing these
symptoms, he was able to function. Other than the discomfort of having a
voice telling you that you’re a loser, he could present “normal”, not talking
about delusions in front of people. Was he unwell? He doesn’t like this term,
but it’s better than others. Yes, but it was equivalent to a persistent cough to
Scott. We didn’t have to worry about the carving knife.
o That idea of the carving knife is often what comes to mind when people hear
the word psychosis. In reality, violence is not a part of psychosis, it’s not in
the DSM-5. Criminal Minds is an obvious example. It all sits on a spectrum,
about how well Scott is or not. Even at Scott’s worst, he would do things like
poking a broom through the ceiling looking for speakers, but Scott waited to
be alone for this. He also took a knife to the lounge. Nothing violent happened
in front of others. This was based on a delusion that had developed for weeks.
This resulted in Scott’s first hospitalisation.
o The idea of a spectrum is immediately different to a categorical designation of
“psychotic”. Symptoms wax and wane. Functioning also slides along a
spectrum. As Scott becomes less well, he is less able to handle day to day
activities, and things become more disorganised, and making appointments
and things becomes difficult.
o Even on medication, this lives on a spectrum continuously. Medication is not a
cure. There’s no cut and dry of being well or unwell, and this applies to
medication. Scott still has his fixed delusional beliefs. The medication quiets
the voices but does nothing for the delusion. While Scott is technically “well”,
he is still impacted by these symptoms. This is far more complex than we may
have anticipated.
o Important to take on the idea of multiple aspects of mental illness co-
occurring. We know that people can experience psychotic episodes, with
anxiety and depression. Depression and anxiety come so often together.
o Fay on co-occurrence: Most people who have considerable lived experience of
mental illness have co-occurring experiences. Recently Fay had a call with a
young man (20) in intense distress because he was so scared that he was going
mad. The anxiety he was talking about was so extreme (which Fay had
experienced), and Fay has also experienced “madness”, like hearing voices
and having hallucinations. The movies are generally very wrong. Extreme
anxiety is harder to live with than madness. It is so bodily and all-
encompassing, when the air around you is tense. Extreme anxiety is so hard to
live with, and people don’t give people enough credit.
o Fay actually doesn’t believe in “mental illness” anymore. There is so many
alternative attitudes that make more sense to her than “illness”. There’s no
blood test or anything that proves you have an “illness”. It is actually just a
response, and a normal response to trauma.
o When Fay becomes “mad” or particularly “unwell” she becomes so paranoid
that she won’t speak, because she’s not sure whether it’s her speaking or
whether it’s the other “beings” or voices that are speaking, and she’s also
worried that people will misconstrue what she’s saying and act against her
well-being by freaking out. Fay will do anything to avoid going back to
hospital. In the past she has found that when she’s really unwell, she has less
chance (strangely) of being hospitalised if she keeps her mouth shut. She can
say yes and no to family, but that’s about it. It’s all on a spectrum.
o Her symptoms involve hearing voices (audibly) and then an inner dialogue
which can be just as crippling. Your own lack of self-confidence and
judgement can be as difficult to manage as the voices. Fay’s voices know her
weakness, and will tell her things like “you’re a shit mother… you shouldn’t
be here… you’re making my family miserable” and usually it is this kind of
degradation of her worth. However, she also had some characters she really
valued that were with her all the time. These characters were trying to “keep
her safe”, who would say things like “don’t talk to this person… cross the
street now.”
o After sexual abuse as a child, this kind of hyper-alertness just becomes a part
of your life and being, and it becomes very hard to trust anyone when you
experience this kind of betrayal.
o Fay’s desire not to speak potentially is indicative of a fear of being
disempowered. There is a power imbalance issue here with clinicians and
people who hold keys to services, treatment and the system. Fay has been
admitted to care against her will, as well as being medicated against her will,
so the fear is a rational one.
o Community treatment order: The Mental Health Act allows for Fay to be
treated against her will in the community after being released. They have to
 keep taking medication while living in the community, otherwise, if they find
out (via blood tests and things), they can be put back into hospital against their
will. If you refuse medication in hospital they can force you to have it and
restrain you.
o These medications are awful. They make you feel really sick, and make you
feel you have cotton wool stuff into your brain and in behind your eyes. They
make you feel separate from others, down a long tunnel away from reality here
and now. They create a different kind of reality that is not nice to be in, on
these medications. For some they work well, but for many, they have such
profound physical and psychological impact that they don’t work well either
in the short or long-term. Big pharma and psychiatry seemed to have
convinced the community (GPs and the like) that they must be on these
medications, that they can’t be well without them, and that they can’t
contribute to society without being medicated and monitored.
o This is just not true, according to Fay. Fay no longer takes medication, and the
only reason she has been able to come off them is because she moved to a
different area and she hadn’t been “mad” in that area. Her new doctor was not
afraid to say that the medication was killing her, and were open to trying
different treatment options, which has completely transformed her life for the
better.
o Fay has been married since 16, contradicting the notion that people with
psychosis can’t hold meaningful relationships. Her health has improved so
much that she is talking about her normal life again with her husband.
o Deinstitutionalisation really coincides with the advent of anti-psychotic
medication, which we normally talk about in a flippant way in academia.
o Scott has had experience with taking additional medications for side effects.
He is on anti-psychotics (injection every 3 months), which he is new to when
his voices became overwhelming. He had developed the side-effect of
akathisia (the inability to remain still). The urge to move is constant, which is
very intrusive, so he was put on PRN to help with that, and now on two
medications. This side-effect medication also has side-effects of its own,
which can lead you to be put on another medication, and this can become a
spiral. Scott knows people on 10+ medications, and half of them are only there
to manage side-effects.
o Fay took 22 tablets a day. Before she was put on to psychiatric medication, she
didn’t even take Panadol. Within 2 months of being put on anti-psychotic
medication and mood stabilisers, she put on 22kg and her physical health
started to deteriorate. She developed a tremor in her hands and legs, and now
takes CBD and THC to manage the tremor, because without it, she can no
longer walk and feed herself or use her computer. This has been caused by the
medications she was on. They hoped that once she was off this medication it
would settle down, but unfortunately the damage has been too profound. The
physical disability is continuing to worsen over time.
o We haven’t yet discussed coping cognitive and behavioural skills to help
ameliorate the voices.

Prac 1

 Essay topic: “DSM anxiety disorders are not genuine states of mental ill-health.”
Must examine at least two issues from below:
 o The prevalence, reliability, and validity of an anxiety disorder diagnosis
o Overlap of anxiety with trait characteristics like neuroticism
o Treatment outcomes and efficacy for anxiety disorders
o Biomarkers and/or behavioural indicators of anxiety
o Contemporary models of psychopathology (e.g. clinical staging, HiTOP,
RDoC)
o The intersection between culture and mental illness (e.g. the effects of de-
stigmatisation initiatives, shifting cultural concepts of mental health and
illness states, cross-cultural variations in concepts of mental health and
illness).
 Should be very argumentative, not that discursive, unless the thesis lends itself to
discussion to make the case. Acknowledge conflicting sources but only if you can
resolve it.

Lecture 2: Models of Psychopathology

 Understanding heterogeneity: People’s life experiences differ. This variability across

individuals extends to states of mental health and illness as does the degree to which
we are resilient against or vulnerable to, the latter. Heterogeneity describes this
complexity and variability across experiences. It manifests across and within
disorders. Reliability is a key concept here in the DSM approach. Clinician A should
come out with the same answer as clinician B. Heterogeneity is a core challenge. How
can we overcome this complexity to reliably determine who is experiencing clinically
significant experiences of mental ill-health?
 The dominant classification systems are the categorical systems of ICD and DSM.
Below is an example of the diagnostic process at its most simple and crude.
 o DSM5-TR Diagnosis example: panic disorder:

o Note that DSM diagnosis does not occur independently of “case formulation”
– understanding clients and their context comprehensively. Read Jackson
(1993) on Canvas. Context allows us to differentiate between disorders, even
when symptoms are similar. We are looking at symptoms in context, not in
themselves.
 Revisiting categorical and dimensional models:
o Three primary approaches to classification of mental disorder:
 Categorical: divides psychological disorders into categories based on
criteria sets with defining features.
 Dimensional: aspects of psychopathology are quantified on a scale. We
know that symptoms are far more dimensional than categorical
(Haslam paper).
 Hybrid: a hypothetical combination of categorical and dimensional.
The DSM5-TR is actually a hybrid model, allowing rating of symptom
severity after the initial diagnosis.
o We want to know what the real situation is for people living with mental ill-
health. Is there clinically significant disturbance? Sometimes there will be
overlap between the clinical and non-clinical population, and this varies in
different cases. Some areas might be easier to distinguish than others. The first
diagram may represent personality disorders, whereas the bottom picture
might represent anxiety.

o It may also be the case that there are more than 2 populations. Maybe there is
one population who are very unaffected, at low risk, and another that live on
the borderline, and a population with more risk with more impactful
experiences. Think of all of this as a hierarchy. Real distributions are

unknown:
o Symptom level hybrid models example of hearing voices: We can approach
pathology at various levels of symptoms, disorders, and latent constructs.
From Baumeister et al. (2017). The evidence did not support the first model. It
supported both second (dimensional) and third (hybrid) models, but there
wasn’t enough evidence to distinguish between them.

o MMPI-2: The Minnesota Multiphasic Personality Inventory is another hybrid

categorical and dimensional model. It involves a survey of over 500 questions
that map onto a number of subscales (on the left), indexing a range of areas of
personality and psychopathology. We can then rate people dimensionally from
mild to severe and document people quite comprehensively. Has self-reporting
problems.
 Vulnerability to disorder: Diathesis-stress models

o For disorder to occur, there must be vulnerability first. In addition to

vulnerability, there needs to be an event or series of events at are adverse,
traumatic, or stressful (but they can still be positive).
o Diathesis: vulnerability, often in terms of personality. For example, neurotic
personality traits. If there are low levels of vulnerability, it may take more
events for disorder to occur. We often talk about pre-disposing factors or
having a pre-disposition. Example:

o Stress: common life events, not just negative ones. We talk about precipitating
factors, the circumstances that have precipitated the presenting problem.
 Models focused on disorder progression: Clinical Staging Model (McGorry et al.,
professor at unimelb)
o The model was adopted from cancer staging (stages reflecting disease, here
disorder, progression). It was based largely on observations by Pat McGorry
and Henry Jackson in schizophrenia and psychosis.
o The focus is on identifying those at risk and facilitating early intervention. The
earlier we put measures in place, the better the outcome.
o This is different from Stepped-care approach: Stepped care is an escalation of
treatment. Clinical staging instead suggests you get treatment according to
stage of disorder.
o Progression of disorder classifications: subthreshold symptoms can be
leveraged as early warning signs of disorder. At every level there are a range
 of factors involved.

o In most cases, mental disorders develop over time with worsening severity.
The staging model aims to define various stages of the development of
disorder and match treatment.
o Preventative focus: the central goal is to stop the emergence of the first
episode of disorder. If complete prevention is not possible, then the aim is to
prevent progression to later stage disorder and prevent worsening and poor
prognosis.
o It also aims to use more universal interventions that are less costly, less
harmful, and less intense at earliest stages.
 Transdiagnostic models of psychopathology:
o These models try to act as a response to the heterogeneity of symptoms across
disorders. Anhedonia, for example, occurs in many disorders. So too with
psychosis. These symptoms are transdiagnostic. This is a central criticism of
the categorical approach.
o Hierarchical taxonomy of psychopathology (HiToP): The idea of having a
taxonomy is a reasonably recent concept in psychopathology in human
history. Emil Kraepelin was first to come up with taxonomy, inspired by
botany.
 o Example of GAD (Generalised Anxiety Disorder):

o Example profile: This is both categorical and dimensional.

 Data-focused models of psychopathology:

o Normative statistical modelling: Normative statistical modelling focuses on
data-informed developmental trajectories. We can determine outcomes based
on a test of where someone is at right now, based on our understanding of
large normative population data sets. We make predictions and can think about
early intervention. See Marquand et al. (2019) on Conceptualizing Mental
Disorders as Deviations from Normative Functioning, Molecular Psychiatry,
 24.

o Research Domain Criteria (RDoC) from Insel et al. (2010): More focused on
research than clinical practice but hopes to inform clinical practice. It emerges
in response to heterogeneity of symptoms within disorders. This was a call to
the research community to start generating data sets to account for this
heterogeneity. Why do even our best treatments work for half the patients we
give them to. Precision treatment is part of the goal.

A ro u sa l/R e g u la to ry S ys te m s
S ys te m s fo r S o c ia l P ro c e s s

o RDoC example:
C o g n itiv e S y ste m s
N e g a tive V a le n c e

P o s itiv e V a le n c e

S e n s o rim o to r

4
2
0
-2
-4

Anxiety Depression
Schizophrenia ASD
 o RDoC exemplified:

o Real-life RDoC: Take heterogenous diagnostic categories and find common

dimensions and subgroups (preferably with Tx implications).

 Biological, psychological and social/environmental models:

o Biopsychosocial models – Biopsychosocial approaches to understanding
mental disorder integrates a range of factors:
 Biological: normal biology, disease processes and genetic influences.
 Psychological: thoughts, feelings and perceptions
  Social/environmental: culture, ethnicity, social environment.

o Biological paradigm includes: genetics; structural brain damage (hard lesion,

abnormalities); disordered physiology (e.g. inflammation processes and
depression); neurochemistry; functional connectivity impairments (e.g.
schizophrenia, soft lesion)
 Genetics: Can lead to ongoing vulnerability.

 Neurochemistry: No single neurotransmitter levels are likely deficient

across the entire brain. Many neurotransmitter levels are likely aberrant
 across multiple brain regions.

 Connectivity-driven classification: Over 10 years of efforts show poor

reliability of within-person functional connectivity networks. We still
don’t know how consciousness happens, and we are dealing with
phenomenological experience. We are way premature on this.

o Psychological paradigm: Beck’s ABC model.

 o Social/environmental paradigm: Can think about a range of determinants of
mental ill-health here. Supportive social relationships are conducive to mental
health.

 Social determinants of mental health

 There is an idea that everything in psychopathology is trauma. From a

scientific perspective, trauma can be instrumental in the onset of
psychopathology. The definition of trauma is expanding, but it does
not account for everything. To argue that transness is illegitimate is
like saying the earth is not round, it has been around forever.
 Cultural models:
o Australian First Nations Model of Social and Emotional Wellbeing: “Culture
can influence Aboriginal and Torres Strait Islander people’s decisions about
when and why they should seek health services, their acceptance of treatment,
the likelihood of adherence to treatment and follow up, and the likely success
of prevention and health promotion strategies.” Australian Government,
 National Aboriginal and Torres Strait Islander Health Plan 2013 - 2023,
Department of Health, Canberra, 2013, p.9.

o Note that geography and memory are intrinsically linked for indigenous
communities. Colonialization has caused a lot of trauma in this regard. This is
a very holistic conceptualisation of mental health.
o They also have a completely different approach to “healing”.
 Case formulation: Whichever the model/s, understanding individuals
comprehensively and contextually is paramount. “In my view, the very raison d'être
for the taking of a clinical case history: it should help describe and contextualise a
person's presenting problem — one that is causing him or her distress. Further, it
should provide a diagnosis and help guide further assessment, aid in the selection of
appropriate treatment(s), and allow some prognostications.” Jackson (1993) – read on
Canvas. Treating individuals with respect and compassion is critical.
 Hearing voices 2: Fay Jackson and Scott Gourlay
o Is health and illness the right way to think about these phenomena? Or is it
more appropriate to think about this from the perspective of human
experiences without assigning a value judgement, and what would be the
implications? Does the label of an illness make us worse?
o Fay: Giving distress (as a result of trauma) a label is unnecessary, it is a
natural and normal response. It is your body trying to protect you. This is not
illness. Trauma can have the feeling of physical illness. Situating our
experiences as an “illness” is a form of gaslighting. The illness lets society off
scot free from the burden of the trauma that triggers mental ill health. It is
response and reaction, not illness.
o From the biopsychosocial perspective, we’re thinking about all the factors that
contribute to this distress response. Fay’s example captured this model,
particularly of a supportive social environment, as her voices subsided when
someone clearly displayed empathy and really listened.
o Fay: Things like trauma can have an impact on DNA. It is still just a trauma
response. Medications can help, but let’s talk about how medication is part of
dealing with trauma. Most mental illness can be traced back to trauma, and we
need to understand that this is the basis of what is happening to them. Fight or
flight responses are not an illness, they are normal responses. In other cultures,
people who “hear voices” are worshipped as shamans. Meanwhile, Scott and
Fay have been forcibly treated, disrespected, devalued, having terrible impacts
on their bodies and psyches. If someone connect with them and sees their
value separate from what has happened to them, that is the answer.
o Scott: Part of his recovery was recognising his role in the abuses he undertook,
recognising his role as the victim, not as someone who did something wrong.
The abuse was buried and hidden away because of guilt, and his voices reflect
that, one is an abuse engine, for example, and another is about other people
(protective but nasty). Schizophrenia didn’t onset in Scott till his 30s (quite
late) following an abuse by 6 other people, completely random. He then
became quite unwell, but it was this trauma that broke the jar effectively. He
couldn’t fit everything back in again. This led to his first psychosis. Trauma is
the big thing, and Scott’s body has had a hyperactive response (like
autoimmune response).
o If we reframe mental illness as a response to trauma, Scott says that it takes
the experience more away from himself. He was told he would never be useful
again, and that he would forever have this condition, and his life was over. He
took this on as a failure on his part, something fundamentally broken. When it
can be put down to a trauma experience, it isn’t Scott that is broken anymore,
it is the experience that was overwhelming. These responses include anxiety,
auditory hallucinations, hypervigilance, paranoia, etc. Scott can now recognise
this as a protective response against the trauma he’s experienced, and he
doesn’t have to carry the blame. He still sometimes blames himself, after 56
years of this negative internal monologue, but it is better.
o CBT wasn’t even offered to Scott when he was first diagnosed with
schizophrenia. It was not considered that it would help at all. Medication was
the only option, otherwise he was told he would hurt people. He had no space
to deal with the trauma at all. His response may be unusual, or more amplified,
but trauma can look like many different things, and everyone responds
differently.
o Both Scott and Fay highlight exactly why categorical ways of thinking about
these things can be so problematic.
o Scott’s account of the implications and process of diagnosis sounds utterly
traumatising and shows how inadequate it is. The diagnosis carried a
completely negative message for him. Scott and Fay are both talking about
symptoms, not conditions. The DSM has really clustered together symptoms
and called them a name, Scott disagrees with this. Talking about experiences
and symptoms is more real for them than the label of schizophrenia.
o Schizophrenia has such negative connotations nowadays. When Scott has
mentioned it to people, they have actually taken a step back. The stigma
attached to this word is crazy. Grabbing a whole bunch of symptoms and
giving them a label seems inaccurate, particularly looking at the causes of
schizophrenia which are so wide and varied. Rather than being a real thing
called “schizophrenia”, it is actually much more likely that what we label is
actually a collection of experiences or symptoms that all happen to present in a
 similar way, never exactly the same, but similar. People with schizophrenia
can also have radically different experiences (not hearing voices, for example),
and there is significant variation. Even in DSM framework, there has been
attempts to sub-type schizophrenia (paranoid, etc.), which is now gone
because the clinical utility was low, and the stigma was completely over the
top.
o Haslam suggests that big data points towards dimensional paradigms, not
categorical, and these boxes don’t really reflect what’s going on with the
science.
o Fay was given similar messages to Scott after diagnosis. She would never
work, and would never be a valuable member of society with meaningful
relationships. She believes we are all born for a reason, and we are all born to
do the best, and her clinician told her she was crazy for believing this. This is
traumatic. Fay was married with children, and was told she might have to give
them up. She met a peer worker, perfectly functioning with the same
diagnosis, who helped her with this. She told her that if I can do it, why can’t
you, and went a step further by challenging Fay, “in fact, what gives you the
right not to function?” This flipped a switch for Fay, that she had to stop being
a victim of what happened to her and the psychiatry model. She saw her
experience in a different light. The way she likes to frame it is to think of them
like kinsuke. This is what a lived experience is like. They can function. They
can take what they’ve learned and have value, supporting others to do that.
They’re experience is gold. They are not broken people, they are people who
have had terrible things happen to them.
o Fay: “Society and the medical model ostracises us. It others us.”

Lecture 3: Anxiety Disorders

 General introduction to anxiety disorders:

o Fear and anxiety: Fear describes feelings that occur when a source of harm is
immediate or imminent, e.g. not knowing answers in the final exam. Anxiety
describes feelings that occur when the source of harm or threat is uncertain or
distant in space or time (anticipatory), e.g. being scared now that you might
not know the answers on the final exam in week 3.
o Threat and neural substrates: Human and animal studies reveal general threat
processing pathways, fear-specific and anxiety-specific pathways, and an
overlap in neural substrates of anxiety disorders. (From Craske et al., 2017,
good for essay). Neurobiology does not fall out as neatly as the DSM
 categories.

o Epidemiology (14 European countries): Looking at 12-month prevalence

(occurrence of diagnosis in population over 12 months)
o Australian epidemiology of anxiety disorders:

o Generic aetiology: (Craske et al., 2017)

o What kind are anxiety disorders?

o DSM-IV vs DSM-5: Ones crossed out are now considered trauma disorders.
 o Generic treatment:

 Specific phobia:
o DSM-5 criteria:

o Cases:
 Alex is a 34-yr old nurse, who has developed a fear of blood. She can’t
look it it, be near it, and even gets anxious if she thinks about it. She
has been relocated to the the mental health unit of the hospital in order
to avoid having any interactions with blood. She does everything she
can to avoid having her own blood drawn (often passing out when it’s
necessary). Specific Phobia? Yes.
 Tim is a 55-yr old New Yorker with a fear of rats. He gets sick at the
thought of them. Tim rides public transportation to work. Given the
 number of rats on the NYC subway, he often takes the bus, but if there
are back-ups, he will take the subway. Specific Phobia? No.
o Epidemiology: Has lifetime prevalence of 3-15%, 8.1% in high income
countries (Eaton et al., 2017).

o Aetiology: Learning theories are heavily implicated in the aetiology of this,

like classical and social cognitive conditioning. We can think of the Watson &
Rayner (1920) Little Albert experiment (good example of fear conditioning,
became scared of white rats). This is learning through association: a natural
response (UCR) is associated with a UCS, where the UCR becomes a CR to
the UCS through repetition, taking on the power of the UCS. Many people
don’t recall experiencing or don’t directly experience the phobic stimulus
(social learning). People can learn indirectly, vicariously through others by
watching them (socially). Some people also overrepresent memories of certain
events.
o Treatment: Exposure therapy which can be in vivo, imaginary, virtual reality,
gradual vs flooding. The stimulus is encountered without the feared negative
event occurring. It is about learning the stimulus does not pose the threat we
think it does. 70-85% of people show significant clinical improvement (Roth
& Fonagy, 2009). Premature termination of therapy is not uncommon
(treatment is very uncomfortable and confronting).
 Panic disorder:
o DSM-5 criteria – Recurrent unexpected panic attacks and for a one-month
period or more of: persistent worry about having additional attacks; worry
about the implications of the attacks; significant change in behaviour because
of the attacks.
o DSM-5 panic attack criteria – A discrete period of intense fear in which 4 of
the following symptoms abruptly develop and peak within 10 minutes:
palpitations or rapid heart rate; sweating; trembling or shaking; shortness of
breath; feeling of choking; chest pain or discomfort; chills or hot flushes;
nausea; feeling dizzy or faint; derealisation or depersonalisation; fear of loss
of control or going crazy; fear of dying; paraesthesias (tingling, pins and
needles).
o Cases:
 Katie, a 27-year old female, goes to emergency department after
experiencing an episode of extreme chest pain, difficulty breathing,
and numbness in her arms. She fears she might be going crazy.
 Nothing is physically wrong with her heart. Panic Disorder? Panic
attack, not disorder.
 Ahmad is a 45-yr old man who has been having episodes of difficulty
breathing, heart racing, sweating, tingling, and feeling like things are
‘unreal’. He’s had about 6 of these in the past month. He’s otherwise
healthy. He’s desperately afraid he may have another one and has
begun avoiding exercise, crowded places, and spicy foods. Panic
Disorder? Yes.
o Epidemiology:
 There is a 13.2% lifetime prevalence of panic attacks. Among those
with panic attacks, 66.5% report recurrent attacks, 4.9% past-year
attack, and 12.8% of those with panic attacks meet criteria for panic
disorder.
 There is 1.7% population prevalence lifetime panic disorder, with
34.5% of lifetime panic disorder patients experienced panic attack in
the past year.
 There is 1.0% past-year panic disorder.
 Most develop panic disorder between 18-29. Women are 1.8x more
likely to develop it than men. Low household income increases odds
ratio to 1.5. (De Jong et al., 2016).

 30-50% of people affected will have agoraphobia (avoidance of

situations where escape would be difficult). 50-60% have lifetime
major depression, with one third with current depression. 20-25% have
a history of substance dependence.
o Treatment: No difference in psychotherapy vs pharmacotherapy (Cuijpers et
al., 2013). CBT, anti-depressants (SSRIs, SNRIs), and benzodiazepines all are
viable treatment options.
 Social anxiety disorder:
o Symptoms:

o Cases:
 Jim hates doing things in front of other people. He always goes out of
his way to avoid social events and has done so since he was an
adolescent. He has a job which requires him to present reports in front
of group, and he often gets colleagues to read his reports for him.
While this causes him trouble at work, his employer doesn’t really
mind; Jim is very good at his job. Social Anxiety Disorder? Yes, but
not sure, maybe personality? Not impacting functioning?
 Sarah will never eat, write, or prepare anything in front of others. She
is too concerned that they are judging her. She has felt this way for the
past several years and it is making her academic life very difficult. She
often has to go home and requires specific assessment settings in order
to complete her assignments. Her marks have been worsening and she
is at risk of failing out. She cannot even think about doing things in
front of other people, it makes her physically ill. Social Anxiety
Disorder? Yes.
o Epidemiology: 4.0% lifetime prevalence; 2.4% past-year prevalence; 1.3%
past-month prevalence. 75% have developed before age 20. 47.0% lifetime
comorbidity with Mood disorder, 59.8% lifetime comorbidity with another
Anxiety disorder, 26.7% lifetime comorbidity with substance use disorder.
38% receiving some treatment.
o Aetiology: Spence & Rapee (2016)

o Treatment: Rodebaugh et al. (2004)

 Exposure Therapy: Assumption – Client must experience the feared
situation to change the affective-behavioural patterns and associative
ideation. Can fail via mental distancing - “it’s just role-play”. Safety
behaviours (rehearsed speaking) can also be maladaptive
 Applied Relaxation: Progressive Muscle Relaxation – may work
 Social Skills Training: Can be helpful if there is a deficit
 Cognitive Restructuring: Changing belief from “I must not appear
nervous when speaking in public” to “I’d prefer not to appear nervous
when speaking in public”. Making the thought less concrete and
absolute, out of an all or none framework.
 Generalised anxiety disorder (GAD)
o Diagnostic criteria: Stein & Sareen (2015)

o Epidemiology: 4-7% of the general population. Typical onset in childhood or

adolescence. Females are at more risk than males 2 to 1. (Will be asked big
picture questions on prevalence, remember rules of thumb).
o Co-morbidity: 90% of GAD patients have at least one other lifetime disorder,
such as panic disorder or depression (not typically neurodevelopmental or
personality disorders, although this is possible). 66% have another current
such disorder. There is a worse prognosis over 5 years than panic disorder.
(This is an important slide for exam).
o Case: A 45-year old male, military veteran, reported being a worrier his whole
life. His parents and family reported that he struggled to make choices about
inconsequential things and every ache, pain, or discomfort led him to believe
he was seriously ill. He worried less when he was in the military; things were
very structured and organized and he had too much to do to waste much time
on the things he used to worry about (structure erases uncertainty and helps
gloss over anxiety, how interesting). Upon return from his deployment, he felt
generally sad, had trouble sleeping, was very irritable, and found himself
needlessly simulating every possible outcome of all his choices in his head. He
felt his thinking pattern was out of control and he would sometimes spend
hours contemplating which television show to watch for the evening, only to
watch nothing and to go to bed. His worry had recently gotten so bad that it
was impacting his work and he was calling in sick on a regular basis. GAD?
Yes.
o A valid disorder? There have been arguments that GAD is merely a waste-
basket diagnosis. Others have suggested that given its comorbidity with
Depression (50-75%), it may merely be a marker for Depression or a Distress
Disorder. GAD is as likely to occur before as after Major Depressive Disorder
(MDD). GAD + MDD more impairing than MDD alone. GAD more likely to
lead to Attention Bias (more future focus) while MDD more likely to lead to
Memory Bias (history focused, rumination).
o Aetiology: Behar et al. (2009)
 Avoidance Model of Worry (Borkovec): “worry = ineffective
cognitive attempt to problem solve and thus remove a perceived threat,
while simultaneously avoiding the aversive somatic and emotional
experiences”. The attempt to solve the problem is ineffective, and
 doesn’t remove it because of avoidance, avoiding the emotional
experience of encountering the problem.
 Intolerance of Uncertainty Model (Dugas & Ladouceur): “uncertain or
ambiguous situations are 'stressful and upsetting’. Belief that worry
will serve to either help cope with feared events more effectively or to
prevent those events from occurring at all”. This one seems most
plausible to me. Tolerating uncertainty is one of the things therapy
often targets.
 Meta-cognitive model (Wells): “People initially develop belief that
worry helps (and perhaps it does), but subsequently begin to worry
about their worrying (meta-worry). Efforts at thought control fail and
people feel helpless.” This also makes sense, but probably insufficient
(but maybe marker of what is characteristic about GAD).
o Contrast Avoidance Model (Newman & Llera, 2011): Worry does not
facilitate avoidance of emotions. Instead, it does sustain negative emotionality
(i.e. restricting affect). If we are always in a state of negative affect, in the face
of adverse events, it doesn’t have as much of an effect. We fear the contrast of
emotions if we weren’t worrying all the time.

o Treatment: Only about 50% of patients respond to medications and/or

psychotherapy (Cognitive Behavioral Therapy) This is a compelling drive
behind initiatives like RDoC, and other data-based projects, trying to uncover
more personalized precision therapy (one area of significant gain in next 20
years hopefully). There is insufficient evidence for meds vs. CBT. Combined
therapy recommended in complex cases. Treatment can be made difficult as a
result of substance use comorbidity (35%), sleep problems comorbidity, and
physical illness comorbidity.
 o Possible medications:

Lecture 4: Mood Disorders

 Overview:
o Depression and mood: Mood refers to a person’s sustained experience of
emotion. Affect refers to the immediate experience and expression of emotion.
Mood is to affect as climate is to weather. Mood disorders (according to the
DSM-5) involve a depression or elevation of mood as the primary disturbance.
They can have other abnormalities like psychosis, anxiety, etc.
o Mood disturbance: unipolar vs bipolar. We spend most time between
hypomania and dysthymia, in a euthymic mood (things are just fine). We will
be referring to this figure a lot in this lecture. Curve is a trajectory over time
 for an example case.

o Mood disorders covered in lecture:

 Depressive disorders: Major Depressive Disorder (MDD); Persistent
Depressive Disorder (PDD).
 Bipolar and related disorders: bipolar I; bipolar II; cyclothymic
disorder.
o Normal human emotion can be characterised by feelings of sadness, despair or
unhappiness. Mood disruption occurs in normal human functioning. Grief, for
example, is an appropriate sadness in response to a recognised external loss. It
is realistic, and appropriate to what has been lost, and is naturally self-limiting
(aka uncomplicated bereavement that tapers off). How can we distinguish
between this and clinical depression? This is a focus of this subject.
o Normal vs clinical depression: Some features of clinical depression
 Intensity: the mood change pervades all aspects of the person and
impairs social and occupational function. “The pain is unrelenting, one
does not abandon, even briefly, one’s bed of nails but is attached to it
wherever one goes” William Styron, Darkness Visible.
 Absence of precipitants: Mood may develop in the absence of any
discernible precipitants or be grossly out of proportion to precipitants.
 Quality: the mood change is different from that experienced in normal
sadness
 Associated features: The mood change might be accompanied by a
cluster of signs and symptoms including somatic and cognitive
features.
 Depressive disorders classification:
 o Hi-Top Transdiagnostic model:

o The Tripartite Model of Depression and Anxiety (Clark & Watson, 1991).
Tries to account for overlap between anxiety and depression in a way that
complements the Hi-Top model.

o We are focusing now in the unipolar section of the mood chart above.
 Major Depressive Episode (criterion that must be met to be diagnosed with the
disorder)
o DSM-5 Criteria – 5 or more symptoms present for more than 2 weeks:
depressed mood; anhedonia; decrease or increase in appetite or significant
weight loss/gain; persistently increased or decreased sleep; psychomotor
agitation or retardation; fatigue or low energy; feelings of worthlessness or
inappropriate guilt; decreased concentration or indecisiveness; recurrent
thoughts of death, suicidal ideation, or suicide attempt. In PDD, we don’t see
anhedonia, characteristic of MDD.
o DSM-5 specifiers: psychotic features (mood congruent or mood incongruent);
melancholic features (very profound, exaggerated features of depression,
extreme sadness, would warrant admission to care); catatonic features (a range
 of behavioural phenomena in response to stimulus); postpartum onset; anxious
distress (feeling on edge); seasonal pattern (Seasonal Affective Disorder
[SAD] or winter depression).
 Major Depressive Disorder (MDD):
o DSM-5 criteria – To meet criteria for a Major Depressive Disorder, the
following must be observed: presence of a Major Depressive Episode; episode
not better explained by another diagnosis; no history of mania, hypomania or
mixed episode (unless substance or medical illness related), in this case we’re
talking about bipolar.
o Epidemiology: Lifetime risk is greater for biological females than males.
Family history of MDD increases risk 1.5-3x. Up to 20-25% of patients with
major medical comorbidity (CVA, diabetes, cancer) will develop MDD. Often
comorbid with one or more anxiety disorders.
o Associated problems: Otto et al. (2016)

o Course (Steinert et al., 2014): 40-60% of depressed individuals exhibit a stable

recovery (complete recovery back to baseline is very rare. As many as 50% of
individuals relapse within 5 years. 15% of individuals exhibit a chronic course
(can be overlap with PDD here). 30-60% exhibit recurrent course.
o Suicide (Turecki & Brent, 2016): As many of 60% of people who die by
suicide have MDD. 12-month prevalence of suicidal ideation is ~2.0%. 12-
month prevalence of suicide attempts is ~0.3%. Around 3500-4000 people die
to suicide a year in Australia (more than roads). Risk factors include: family
history; early life adversity; psychiatric ollness – esp depression, anxiety (90%
of those who suicide); impulsivity; substance misuse; sense of
hopelessness/helplessness.
o Suicide risk: This used to be lecturer’s key area of practice. Stopped after
brother died to suicide. We would want to avoid where and how a suicide took
place in media and in discussion. Should be no indication of means. The
Werther effect is also important here, where the protagonist of the book dies
by suicide, and it was observed people who shared demographic
characteristics of the protagonist were dressing like him when they died. When
Amy Winehouse died, there was a similar effect. If they can’t make it (and I
 am similar) how can I? Access to support is key.

o Treatment – psychotherapy(Otto et al., 2016): We’re looking at psychotherapy

of pharmacological intervention. Generally CBT is one of the better ones.
Behavioural activation therapy targets depressive behaviours (bed-lock).
 o Treatment – pharmacological (for more severe experiences): The big 3
hormones being modulated are serotonin, dopamine, and noradrenaline.

 Persistent Depressive Disorder (PDD):

o DSM-5 criteria:
 A. Depressed mood more days than not for at least 2 years.
 B. Presence of 2 or more of the following: change in appetite or
weight; change in sleep; low energy or fatigue; low self-esteem (not in
MDD); poor concentration or difficulty making decisions; feelings of
hopelessness. Previously dysthymia, low level, chronic depression. It is
a proposed alternative to recurrent MDD.
o Treatment: Generally, the same as MDD. It is more likely to be treatment
resistant. Physical and psychiatric comorbidities are common. Undertreatment
is likely as many people present to GPs (who fail to diagnose this) and the
experience is more ongoing (feels like just the way they are).
 Aetiology of depressive disorders:

o Genetics: Heritability of unipolar depression is high, around 40-70%. First-

degree relatives of depressed individuals have risk of 5-25%.

o Neurobiology: A number of neural regions are implicated, including the

hippocampus. There are suggestions of alterations to dopamine, serotonin and
noradrenaline.

o Immune system: Some forms of depression may be related to immune activity.

Enhancing inflammatory response leads to depressive-like experience. Brain
inflammation may account for part of the story. Anti-inflammatory
 medications may be helpful. This may only be relevant for a subset of cases.

o Stress: Stressors are 2.5x more likely in depressed patients. 80% of MDEs are
preceded by major life event (especially loss). Stress often leads to more

stress.
o Personality: Neuroticism is linked to depression (and also anxiety).
Introversion is also linked to depression. Negative self-esteem/poor self-
scheme is also linked to depression. Interpersonal sensitivity may be a risk
factor.
 Models of depression:
o Behavioural model of depression: Based on conditioning mechanisms around
behaviour, and in depression, we exhibit low rates of behaviour. It is a
downward spiral. Uses operant conditioning.

o Beck’s cognitive model of depression: A schema (beliefs, rules and

assumptions) are based on early experience. Negative events establish
negative/dysfunctional schema. Critical incidents trigger negative schema
which govern information processing. Activation of the negative schema leads
to negative automatic thoughts (NATs).
o The ABC Cognitive Model of Emotion and Behaviour: CBT focuses in on the
belief.
 A = activating event: What was happening when negative feelings
were experienced?
 B = belief: Beliefs or thoughts about the activating event.
 C = consequence: Involves feelings (emotions and physiological
experience of emotion) and behaviour performed.
 Example:

o CBT for depression: After thorough assessment (includes symptom set,

severity and suicidality), there are phases of therapy:
 First phase: Focuses on behaviour. Treatment often includes a
concentration on psychoeducation and non-cognitive (behaviour)
techniques. Relatively straightforward/structured and easier to achieve
successes (people who are depressed experience difficulty initiating
change). It is about behavioural activation aimed at increasing rates of
behaviour (organising schedule, making plans to do things, reinforcing
behaviours).
 Second phase: Treatment focuses on cognitive techniques and
problem-solving.
 Third phase: Generalization of skills learned in therapy and relapse
prevention (warning signs, seeking help).
  Dysfunctional Thoughts Records are often used:

 Bipolar disorders: We are now thinking about the entire spectrum of the mood chart
above, including mania and hypomania. We will discuss bipolar 1 and 2 and
cyclothymic disorder.
o Mania: Abnormally and persistently elevated, expansive or irritable mood.
This expansive quality of mood is characterised by unceasing and
indiscriminate enthusiasm for interpersonal, sexual or occupational
interactions. Symptoms of a mania include: inflated self-esteem (ranging from
uncritical self-confidence to delusional intensity grandiosity); decreased need
for sleep; pressured speech; racing thoughts; distractibility; increase in goal-
directed activities; psychomotor agitation. Example: “When I am high I
couldn’t worry about money if I tried. So I don’t. The money will come from
somewhere; I am entitled; God will provide…During one spree in London I
spent several hundred pounds on books having titles or covers that somehow
caught my fancy: books on the natural history of the mole, twenty sundry
Penguin books because I thought it could be nice if the penguins could form a
colony. Once I think I shoplifted a blouse because I could not wait a minute
longer for the woman…in front of me in line. Or maybe I just thought about
shoplifting, I don’t remember, …I imagine I must have spent far more than
thirty thousand dollars during my two major manic episodes...”  Kay Redfield
Jamision, An unquiet mind: A memoir of moods and madness. This is an area
of psychological disorder where distress is not part of the picture (but it can
be), but usually people are feeling great.
o Mania vs hypomania: In Bipolar I, there are full-blown manic episodes and
potentially MDEs. In Bipolar II, there are definitely MDEs with hypomanic
 episodes.

o Manic episode DSM05 criteria:

 A. A distinct period of abnormally and persistently elevated, expansive
or irritable mood, lasting at least 1 week (or any duration if
hospitalisation necessary);
 B. During the period of abnormality, 3 or more of the following
symptoms have persisted (4 if mood is only irritable) and have been
present to a significant degree: impaired regard for consequences;
agitated, excessively goal directed; flight of ideas; distractibility;
inflated self-esteem or grandiosity; decreased need for sleep
 C. The mood disturbance causes marked impairment in social or
occupational functioning or necessitates hospitalization to prevent
harm to self or others, or there are psychotic features.
o Hypomanic episode DSM-5 criteria: Like manic episode, but not to the same
level or extent as in mania.
 A. Abnormally and persistently elevated, expansive, or irritable mood
and abnormally and persistently increased activity or energy, lasting at
4+ consecutive days.
 B. During this period, three (or more) of the following symptoms have
been present: inflated self-esteem or grandiosity; decreased need for
sleep (e.g., feels rested after only 3 hours of sleep); more talkative than
usual or pressure to keep talking; flight of ideas or subjective
experience that thoughts are racing; distractibility (i.e., attention too
easily drawn to unimportant or irrelevant external stimuli); increase in
goal-directed activity (either socially, at work or school, or sexually) or
psychomotor agitation; excessive involvement in activities that have a
high potential for painful consequences (e.g., engaging in unrestrained
buying sprees, sexual indiscretions, or foolish business investments).
o Bipolar diagnoses:
 Bipolar I Disorder (BP1): one or more manic episodes usually (but not
always) accompanied by major depressive episodes.
 Bipolar II Disorder (BP2): one or more depressive episodes
accompanied by at least one hypomanic episode.
  Cyclothymic disorder: at least 2 years of numerous periods of
hypomanic and depressive symptoms that do not meet threshold for
manic or depressive episodes.
o Epidemiology: Relatively low-prevalence disorder. Bipolar I has lifetime
prevalence of 0.6%. Bipolar II has lifetime prevalence of 0.4%. Bipolar
spectrum has lifetime prevalence of 2.4%. The age of onset is around 20, and
there is not usually a single episode (5.9%) or continuous presentation of
features (17.9%). Multiple episodes are common.
o Clinical picture:
 During manic episodes: elevated or irritable mood (95.5%); excessive
activity (93.7%); racing thoughts (91.1%); reduced need for sleep
(90.2%).
 During depressive episodes: dysphoria with anhedonia (79.5%);
suicidal ideation (78.6%); loss of energy (68.7%); poor concentration
(64.3%); initial insomnia (58.0%); diminished libido (58.9%).
o Clinical picture specifiers: mixed features (depressive and manic features
present during same episode); anxious distress (significant anxiety); catatonia
(unusual movement); melancholic features (profound sadness); rapid cycling
(poorer prognosis).
o Relationship to psychosis (Morgan et al., 2005): Australian Survey (n=112
pt’s w/ Bipolar Disorder) showed: 89% had experienced psychotic symptoms;
20.5% experienced hallucinations; 85.7% had experienced delusions.
o Course of illness: Distinct manic and depressive phases vs. mixed
presentations, i.e., some manic and some depressive symptoms together. Clear
restoration of functioning in between episodes not uncommon. Some
exhibiting rapid cycling – difficult to treat. If untreated, four findings are very
consistently reported: The length of normal periods between episodes
decreases; the length of each episode increases; depressed phases become
more likely; suicidality a major risk factor.
o Aetiology of bipolar:
 o Treatment of bipolar: Mood stabilisers or antipsychotics are common. CBT is
also effective, but not by itself.

Prac 2

 Main criterion for each anxiety disorder:

o Specific phobia: Marked fear, anxiety or avoidance of circumscribed objects
or situations.
o Panic disorder: Concern or worry about having more panic attacks or
maladaptive behavioural changes.
o Agoraphobia: Marked fear, anxiety, or avoidance of situations such as public
transportation, open spaces, enclosed spaces, lines or crowds, or outside the
home.
o Social anxiety disorder: Marked fear, anxiety or avoidance of social
interactions and situations in which one is scrutinised, or situations in which
one is the focus of attention.
o Generalised anxiety disorder: Excessive anxiety and worry about various
events that have occurred more days than not for at least 6 months.
 Common features of anxiety disorders:
o DSM-5: Response is out of proportion to any actual danger.
o 6 months duration (Specific Phobia, Social Anxiety Disorder, Agoraphobia,
Generalised Anxiety Disorder, not Panic Disorder)
o Not due to general medical condition.
 Case 1:
o Symptoms: Restlessness; shaky speech; avoidance of eye contact; avoidance
of social interaction; anhedonia; self-deprecation; cold sweating; paranoia;
delusion; believes in her own incompetence; rumination on others’ opinions;
described panic attacks (not disorder).
o Functional impairment: can’t get work (turning jobs down); social
impairment; unable to concentrate;
o Other? 5 or 6 years duration; introverted personality (neurotic?); using the
body as coping mechanism (holding on); agoraphobia;
 Case 2:
o Symptoms: put together, coherent speech; mood swings; reactions out of
proportion to stimulus; anhedonia; rumination (loud room of his head);
o Functional impairment: symptoms experienced for more than 20 years
(becomes part of life); sought out help 7 years ago; impulsivity;
o Other: GAD; chronic depression; on medication; video part of a campaign.
 Bipolar:
o Euthymia: Stable, not elevated but not depressed mood either.
 o Hypomania: Not quite mania, but a sense of capability and confidence (out of
normal range)
o Mania: very flighty, reckless, on top of the world
o Dysthymia: lowered affect, sense of being blue, slower (out of normal range)
o Depression: Mood is completely flat.
o Diagram:

o Bipolar 1: Mania (shorter episodes, a few days)

o Bipolar 2: Hypomania and depression (episodes spanning a week or two)
 Case study of Major Depressive Disorder: DSM-5-TR criteria:
o A: Five or more of (over two-week period):
 1: Depressed mood most of the day;
 2: Diminished interest/pleasure in activities (anhedonia);
 3: Appetite/weight disturbance (loss/gain);
 4: Sleep disturbance (insomnia/hypersomnia);
 5: Psychomotor disturbance (agitation/retardation);
 6: Fatigue, loss of energy;
 7: Feelings of worthlessness or excessive guilt;
 8: Diminished ability to think or concentrate;
 9: Recurrent thoughts of death or suicidal ideation
o B: The symptoms cause significant distress or impairment in social,
occupational, or other functioning
o Notice how many of these are very cognitive.
 Centre of CBT is that there is always the thought, and it always starts with a thought.
The aim is to pick out the thought and unpack it.
 Bipolar disorder case studies:
o DSM criteria for manic episode in bipolar:
 A: A distinct period of: abnormal & persistent elevated, expansive,
irritable mood; abnormal & persistent increased activity or energy,
lasting >1 wk and present most of the day, nearly every day (or any
duration if hospitalization is necessary).
 B: Three or more of: 1: Inflated self-esteem or grandiosity; 2:
Decreased need for sleep; 3: Talkativeness / pressure to keep talking;
 4: Flight of ideas / racing thoughts; 5: Distractibility; 6: Increase in
goal-directed activity; 7: Excessive involvement in activities with high
potential for painful consequences
o Video of depressive episode: delusion (occurs during depressive episodes);
grandiosity; hallucination (auditory); scattered thoughts; long pauses in speech
without context; diminished ability to think or concentrate; retardation;
fatigue; dizziness; she started singing “On top of the world”;
o Video of manic episode: very talkative and confident; more intense emotions,
irritability (anger, violence); racing thoughts; delusion; pressure to keep
talking; giggling; much faster speech.
o She would probably be diagnosed with Bipolar 1, as she looked like she had
proper mania.
o Take-aways: Bipolar (1) disorder comprises two different (polarized)
experiences: manic episodes and typically (but not always) depressive
episodes. Both depression and manic episodes are abnormal (extreme) in their
experience. Both depression and manic episodes can cause significant
disruption to a person’s life.

Lecture 5: Culture and Psychopathology

 Final exam won’t assess weeks 1-4. Remember it is in person.

 Culture:
o Culture and psychopathology: When psychiatric assessment fails to take into
account sociocultural factors it risks misdiagnosis and the perpetuation of
clinical stereotypes based on race, ethnicity, gender, religion or sexual
orientation (among other factors). We might miss a valid experience of a
disorder, or alternatively, pathologize something that is not a disorder. This is
well-described in literature.

o Cultural considerations in the clinical practice: cultural identity of the

individual; cultural explanations of the individual’s illness; cultural factors
related to psychosocial environment and levels of functioning; cultural
elements of the relationship between the individual and the clinician.
o Cultural syndrome (beyond DSM-5 or any other framework): A cluster or
group of co-occurring relatively invariant symptoms found in a specific
cultural group, community, or context. The syndrome may or may not be
recognised as an illness within culture (e.g. it might be labelled in various
ways), but such cultural patterns of distress and features of illness may
nevertheless be recognisable by an outside observer. (Lol, is anxiety our
cultural syndrome, or pathological competition).
o Cultural syndrome example – Ataque de nervios: A syndrome among
individuals of Latino descent. It is characterised by symptoms of intense
emotional upset, including acute anxiety, anger, or grief; screaming and
shouting uncontrollably; attacks of crying; trembling; heat in the chest rising
into the head; and becoming verbally and physically aggressive. It is
sometimes, but not always, a dissociative experience (e.g. depersonalisation,
derealisation, amnesia), seizure-like or fainting episodes, and suicidal gestures
are prominent. This is very acute and abrupt.
o Cultural syndrome example – Khyâl cap: A syndrome found among
Cambodian people both in Cambodia and internationally. Common symptoms
include those of panic attacks, such as dizziness, palpitations, shortness of
breath, and cold extremities, as well as other symptoms of anxiety and
autonomic arousal (e.g., tinnitus and neck soreness). Khy'l attacks include
catastrophic cognitions centered on the concern that khy'l (a windlike
substance) may rise in the body—along with blood—and cause a range of
serious effects (e.g., compressing the lungs to cause shortness of breath and
asphyxia; entering the cranium to cause tinnitus, dizziness, blurry vision, and a
fatal syncope). The treatment is called “coining” (rubbing a person’s skin with
a coin such that a person’s skin is raw).
o Often, we find that once people leave a culture, the syndrome expression can
be weaker or less prevalent. (Surely we learn something from this). This is not
the case for all syndromes, however.
o Aboriginal Australian culturally-bound syndromes (Pilbara and Perth regions)
(Westerman, 2021): This is a very deep spiritual connection, whose
complexity is very much outside our access.
o Longing for country: This is much more holistic than our approach. Problems
associated with spiritual disconnection Aboriginal people experience when
removed from traditional lands. “Symptoms” can include: physical ill-health,
including weakness, nausea, general “sickness” and somatic complaints;
spiritual ill-health; cognitive disorientation, dissociative fugue (finding
yourself somewhere without remembering how); cultural “ill-health”
including identity confusion, disorientation, acculturative stress (taking on the
way other cultures express psychological distress, likely for people in
metropolitan areas). Appropriate intervention included returning to country to
reconnect with land, culture, and spirit. Participants spoke of knowing when
they needed to return home and this was often precipitated by feelings of
 sadness, despondency, moodiness, frequent crying, wanting to be alone and
arguing with loved ones for no apparent reason. Participants described going
home as feeling like “a rejuvenation” (Westerman, 2021).
o Cultural idioms of distress: A linguistic term, phrase, or way of talking about
suffering among individuals of a cultural group (e.g., similar ethnicity and
religion) referring to shared concepts of pathology and ways of expressing,
communicating, or naming essential features of distress. This is important to
understand because otherwise we might miss expressions of distress from
people from other cultures.
o Example of cultural idiom – Kufungisisa: “Thinking too much” in Shona
(Zimbabwe). As an explanation, it is considered to be causative of anxiety,
depression, and somatic problems (e.g., “my heart is painful because I think
too much”). As an idiom of psychosocial distress, it is indicative of
interpersonal and social difficulties (e.g., marital problems, having no money
to take care of children).
o Cultural explanation or perceived cause: A label, attribution, or feature of an
explanatory model that provides a culturally conceived etiology or cause for
symptoms, illness, or distress (e.g., ‘maladi moun’ – Haiti; or being
sung/pointing the bone – Australian Aboriginal culture, the idea of being sent
distress). Causal explanations may be salient features of folk classifications of
disease used by laypersons or healers.
o Example of cultural explanation – Maladi moun: Literally “humanly-caused
illness”, also referred to as “sent sickness”. An explanatory model that
proposes that interpersonal envy and malice cause people to harm their
enemies by sending illnesses such as psychosis, depression, social or academic
failure, and so on.
o Culture and symptom expression example – psychosis: Visual hallucinations
more common in developed than developing cultures, more in metropolitan
than rural; paranoid delusions (e.g. of being monitored) more common now
whilst delusions of wealth and grandeur more documented during 1930’s in
US.
o Culture and hearing voices: For auditory verbal hallucinations (AVH),
phenomenology and cultural responses vary considerably. In Western settings
(the US), hearing voices is more distressing, and they are more malevolent and
hostile. In India, you are much more likely to have a more productive voice
(telling the person to feed themselves), rather than saying something critical.
This is because of cultural explanation for the voices. In the Western world,
we pathologize voice hearing, equating it to madness. In other cultures, we
may see other explanations, like being visited by spirits of ancestors, or
represent a connection to the spiritual worlds. Rather than being pathologized,
these people might be revered. This is the case for Indigenous Australian
cultures. Describing the rich tapestry of this in Indigenous culture represents a
huge piece of work for psychology. The way symptoms play out can be a
reflection of culture. CBT for hearing voices doesn’t work directly in aiming
for a decrease in the severity or frequency of voices, but instead reframing the
relationship to the voices and decreasing the distress associated with the
voices, trying to understand them as something meaningful, working against a
distressing appraisal of the voices. As a secondary effect, we tend to see
voices to fall off. Some people do not want their voices to disappear. Paper for
this draws data comparing the USA with Africa/Asia about the explanation of
 voices, and the US and India (Ghana) in terms of distress vs. command-order
AVH phenomenology. For example, the Masai in Kenya have culturally
sanctioned periods of AVH, as it is expected to hear voices when a loved one
has died (mentioned in Westerman paper). If they hear voices at another time,
that indicates the person is unwell. Interestingly this is empirically supported,
as it is found that it is more common hallucinate during this time (some
explain as an unconscious vigilance for the person who is no longer there).
 Stigma
o Origin of the term “stigma”: “Stigma” originated with the ancient Greeks
(people marked with “stig”), who physically branded criminals, slaves or
traitors in order that they may identified as undesirable or avoided (Goffman,
1963). They are othered, and thus disempowered.
o Mental Illness Stigma Framework (Fox et al., 2019): Stigma is very complex.
There are many different mechanisms. There are a range of intersectional
factors that mediate the relationship between these things. Other cultural
factors (race, gender, sexuality, success) may all play a role here. We are all
affected by stigma.

o Perspective of the stigmatiser:

 Public stigma (plural or personal stigma) refers to stigma exhibited by
the public towards those with a mental disorder. Public stigma
manifests in three ways: stereotyped attitudes and beliefs, e.g. someone
is “less than” manifested through devaluing language (cognitive);
prejudicial affective responses, e.g. fear, anger; discriminatory
behaviours, e.g. the avoidance of interaction or social exclusion. This
stigma is thought to be particularly harmful, and the driving force
behind other aspects of stigma.
 Pat Corrigan’s Social Attributional Model of Stigmatisation (Groot,
2021). Stigma is elicited by signs of mental illness. Different signs or
“signals” elicit different types of stereotyped and affective reaction, but
the end point tends to be similar (social distancing). Stigma involves
 decontextualized pairings in the way depicted below.

 Structural stigma: Refers to ingrained stigma manifest at the societal

level. Structural stigma is maintained by societal institutions
(government, religion, private) through policy, law, and prescribed
ideologies that restrict opportunities for particular groups. It varies
considerable across societies, time periods and topics. This applies to
mental illness, but also extends beyond to other issues. For example,
HIV-AIDS in the 1980s. The relative under funding and lack of
resources to combat mental health in Australia could be viewed as an
example of this.
o Perspective of the stigmatised: Multiple stigmas affect persons living with
mental ill-health. Individuals living with mental ill-health are affected by
numerous complex mechanisms of stigma. These mechanisms are invariably
outcomes of public stigma about mental ill-health. The Mental Illness Stigma
Framework (Fox et al., 2017) outlines that they include perceived stigma,
experienced stigma, anticipated stigma, and self-stigma.
 Perceived stigma: Is experienced by members of the public living
either with or without mental ill-health. The term refers to individuals’
awareness and perception of public stigmatised stereotypes, prejudicial
emotions, discriminatory behaviour or practices, and/or stigmatised
structural practices. They are distinct from one’s own beliefs. Research
shows that we believe that other people are more stigmatised than
ourselves. Individuals living with mental ill-health are reported to
show higher levels of perceived stigma than those unaffected by
mental health problems. Perceived stigma shares a positive relationship
with symptom severity for those living with mental ill-health (Fox et
al., 2017; Freidl et al., 2008). Perceived stigma is a fundamental
substrate of the anticipation and internalisation of public and structural
stigma. It is our awareness of stigma in culture.
 Experienced stigma: Refers to the experience of having been the target
of expressed negative stereotypes, prejudices and manifest
discrimination related to one’s mental ill-health. May occur in subtle
and insidious terms such as chronic exposure to commonplace
 stigmatising representations of people with mental ill-health in mass
media, or in more acute ways such as the experience of being denied of
significant housing or employment because of one’s mental ill-health
(Fox et al., 2017; Groot et al., 2020). This can contribute to
withdrawal from future opportunities and shares a relationship with the
anticipation of stigma (Fox et al., 2017; Groot et al., 2020; Link,
1987). 
 Anticipated stigma: Is defined as the extent to which individuals living
with mental ill-health expect to experience stereotyping, prejudice, and
discrimination in the future because of their mental health status. It is
central to the experience of anticipated stigma is an awareness of
public and structural stigma, and how this affects people living with
mental ill-health in contexts that are relevant to the self (Fox et al.,
2017). This commonly results in withdrawal from opportunities for
people living with mental ill-health (Groot et al., 2020; Link et al.,
1997).
 Self-stigma: Corrigan’s model – if we are aware of stereotypes and
agree, we will apply them to ourselves. This leads to poorer outcomes,
treatment-participation and seeking.

 Examining the experiences of people living with mental health issues: Our Turn to
Speak and the National Stigma Report Card
o About Our Turn to Speak: Our Turn to Speak was a national survey that
sought to understand the life experiences – whether positive or negative – of
people living with severe and complex mental health issues in Australia. We
wanted to understand if and how a person’s experience of mental health issues
impacts the way they are treated by others in different areas of their lives. This
has now been replicated internationally.
o There were just under 2000 participants (Australian residents aged 18 and
over) living with at least one of the following severe and complex mental
health issues over the 12 months prior to taking part: schizophrenia spectrum
disorders; bipolar and related disorders; personality disorders; obsessive-
compulsive and related disorders; post-traumatic stress disorder; dissociative
disorders; eating disorders; severe and treatment-resistant depression and
anxiety requiring multi-agency support. Our Turn to Speak sample retained for
 analysis comprised N = 1912 participants. Participants were aged 39.21 years
on average (SD = 12.82, range = 18-86 years). They came from all across the

country:
o Experiences of stigma and discrimination: Looked at 14 areas of life about
their experience in the last 12 months.
o Stigma and discrimination in relationships:

I have been treated unfairly

in my role as a parent or
caregiver to my child(ren)

I have been treated unfairly Strongly Agree

by my family Agree
Slightly Agree
I have been treated unfairly Slightly Disagree
by my intimate partner(s) Disagree
Strongly Disagree
I have been rejected by or
estranged from my friends

0% 50% 100%
o Withdrawal from opportunity in relationships:

I expect to be treated unfairly when starting a family or having a child/children

I expect to be treated unfairly by my family Strongly Agree

Agree
Slightly Agree
Slightly Disagree
I expect to be treated unfairly when dating or in intimate relationships Disagree
Strongly Disagree

I expect that people will not want to be friends with me

0% 50% 100%
o Effective approaches to stigma reduction: Approaches to stigma that are well-
established to be effective include: contact (being in contact with someone
with a mental illness), which is positive for both parties and particularly
effective for addressing stigma in adulthood; education (being educated about
mental illness). This makes sense, as familiarity with mental illness is well-
established to be associated with decreased stigmatised attitudes and beliefs.
 o Education and mental health literacy: Education about mental illness
influences stigma reduction by increasing knowledge and understanding of
mental disorders, biological contributions and blame attributions. It
importantly dispels myths about mental illness, for example the violence myth
that invokes fear and a sense of dangerousness. Opening societal discourse
decreases self-stigma. Observing that it is okay to experience and talk about
mental illness. This in turn increases the likelihood of help-seeking, and in
turn, recovery.
o However, it is all about balance. The wrong type of education can increase
stigma. The key is how mental illness is explained. For example, a heavy
psychosocial explanation of mental disorders leads to an increased perception
of blame (people with mental disorders are more to blame for their situations).
Alternatively, a heavy biomedical explanation leads to increased perception of
uncontrollability and immutability of mental disorders (negative stereotypes).
We need a more holistic and balanced biopsychosocial explanation of mental
disorders, such that the negative effects of each approach in isolation are
cancelled out.
o What is happening in MSPS right now with this research? MSPS Mental Ill-
health stigma lab projects: National Stigma Report Card V2.0; Symptoms
stream; Teleweb Service BPD Stigma; News reporting and stigma; Hearing
Voices project; Motivations to stigmatise; Podcast intervention; Psychosis +
alcohol and other drugs; Messaging strategy intervention trials; BPD in mental
health system; BPD in relationships.
o Previous PSYC30014/now MISTLab students: Kelton Hardingham - Capstone
2016, Honours 2017, PhD 2021; Beth Hobern – Honours 2018, RA 2019, PhD
current; Jessica Westfold, Honours 2018, Clinical Masters 2019; Ellen Rankin,
Honours 2019; Emma Waldron, Honours 2018, Mengie Cai, Honours 2020,
Alsa Wu, Honours 2021, Elise Carrote, PhD current; and 2022 Masters
students Ernest Wang, Ashley Milosevska, Kayla Matisi and Robyn Young.
2023 Masters students x 5.
 Learning outcomes:
o Culture:
 Describe important cultural considerations as regards psychopathology
and clinical practice?
 Understand what cultural syndromes, idioms and explanations are, and
describe examples
 Describe how culture affects psychopathology
o Stigma:
 Describe what stigma is
 Identify various stigma processes
 Understand the significance of stigma for individuals with lived
experience
 Describe methods to understand and reduce stigma
 Hearing Voices 3: Alan Thorpe
o He is the CEO of Dardi Munwurro, First Nations organization supporting
indigenous people around mental health and wellbeing.
o Alan: He is from the Gunnaikurnai nation in East Gippsland. His Grandma
was born on a mission there.
o What does “healing” mean from an Indigenous perspective? What does Dardi
Munwurro do? It is a big conversation about how these people escape the
oppression they’ve been boxed into for generations. It is about generational
trauma and shame embedded in spirit. It is about finding places of safety to
talk about that intergenerational stuff. It has been so many events of trauma,
but it is about creating a supportive environment to express this oppressive
stuff like racism, that has ostracized indigenous people from the community.
This is very freeing. Being oppressed feels heavy, and it is like letting the lid
off a cage, releasing the spirit. Sometimes we have to regress to this place. He
went back to the place his ancestors were massacred, and he felt he needed to
be there. This is important in a place where you’re just told to move on, and
this is part of the oppression.
o What are the areas of shame being talked about? Alan: Society has put this
shame on Indigenous people. Before 1967, they weren’t even seen as human
beings. They were invisible. Humans like to be seen and felt. Indigenous
people have been robbed of this. This is only 50 odd years ago.
o Chris: There were literal human zoos. We are talking about a genocide here.
The impact would be enormous, because as a non-indigenous person, it is hard
to even think about this it is that devastating. These effects echo through
generations. Intergenerational trauma is a risk for wellbeing and mental health
for these people. Particularly when the current society still has racism
systemically embedded in it. Chris spoke to an elder who told him that young
indigenous men are already anxious just going to the shops, due to the
anticipation of discrimination and stigma.
o Alan: This made Alan think of his Grandmother. People were taken away and
locked up, separated from spirit and country. They were completely isolated (a
huge risk factor). They still operate the mission, but it is about the way it was
done. This is only two generations ago. He is still grieving, even just talking
about it. The isolation has a ripple effect. It is embedded in the way of
thinking.
o Chris: Lecture looked at a First Nations model of wellbeing, and every aspect
of the model had the term “connection” in it. Connection to country was one
of the main considerations emphasized. Lynn Kelly is an Indigenous author
doing work around Indigenous memory systems and songlines. Uncle Cole
talked about taking young Indigenous men to a spiritual place. This really
opened Chris’ eyes to just how cruel removing people from country was.
o Alan: The sacredness of the land is so deep, as well as the systems in place
pre-colonisation. They are the oldest living culture in the world. How his
ancestors survived and communicated would have been so fascinated. It is
about creating a safe environment, but also trying to get the spiritual energy
right, and recreate some of this cultural stuff. The native plants around the site
help. The elements are really important. This is the connection. Alan loves this
space, he feels really present, away from technology and connecting with
people.
o Alan: Part of your identity is connecting to country. He goes back home and
feels his ancestors, and loves listening to creation stories from wise people that
can share that with him. Creation stories are a large part of this conception of
connection to country. Country is “God”. Their creator is the pelican, and so
he feels a deep spiritual feeling around pelicans. His personal totem is a sea
eagle, that guides him. When you connect with it, it often appears in the sky.
 Indigenous people used to talk about it and be diagnosed. Speaking about
cultural issues has been historically pathologized.
o Chris: The lecture highlights this problem. Our classification systems may not
apply in other cultures. Spiritual connections should not be interpreted as
delusion. We need to acknowledge how much we don’t know as clinicians. In
the lecture we talked about cultural idioms (different ways of talking about
distress that vary across cultures). Students should be mindful of ways of
talking about mental health issues that are not common across cultures.
o Alan: He likes healing work, and the idea of trauma. Alan is into embracing
feelings as an energy. Labels can be burdens for people. It is about the events
that have happened in life and across lifetimes. Alan avoids labels. Part of the
oppression is a lack of spiritual connection and emotional connection. Looking
at the Western constructs, it is about having failed and growing up.
o Chris: Real emphasis on feelings. In the West, the emphasis a lot of the time is
on thinking (CBT for example). Connection to community and ancestors and
spirituality are so intertwined. It is experienced and approached through the
feeling. This ties into the healing approach, doing smoking ceremonies and
such.
o Alan: Part of the healing is feeling. This is what has been suppressed and
taken away from these people. The spiritual connection is such a big part of
wellbeing. Western constructs take this away. We all want to feel loved, and it
is about how to embody this in a society that doesn’t allow you to. All they
want is the connection.
o Chris: Take away should be a mindset that there is so much to learn from First
Nations people about what mental health and ill-health is for them. This has to
be an ongoing journey.
o Alan: Took an indigenous kid into the community space, where the elements
are, and his whole energy and feeling shifted. He was fascinated about how
powerful this can be. The physical environment, and how they set up the
space, is really important.
o Chris: The implications for mental health services are profound. If the
environment is not designed with that factor in mind, facilitating connection to
elements and country, this is a problem.

Lecture 6: Lifestyle Factors and Mental Health

 Lifestyle factors play an important role in mental health, such as: eating healthy food,
physical activity, smoking cessation, alcohol and other drug abstinence, sleep, and
social connections. It is up to clinicians to treat clients holistically and take these
factors into account (rather than just CBT, particularly with substance abuse). We
often need to treat something like alcohol abuse before starting CBT. This is a bit of
background as to why lifestyle is important.
 In 2021, the Royal Australian and New Zealand College of Psychiatrists (Malhi et al.,
2021) published their clinical practice guidelines for mood disorders (read section
6.1), about actions, and lifestyle behaviours people can engage in. These guidelines
are quite ground-breaking, putting these factors into words. Below is an example of
 the guidelines for exercise, as well as the general introduction to the section:

 Behaviour change: This is what lifestyle change looks like in practice. “The universe
doesn’t give you what you ask for with your thoughts; it gives you what you demand
with your actions” (Steve Maraboli). It is important for clinicians to make clear to
patients that wellbeing is not something we just have; it requires deliberate,
considered, and action on our part to foster and maintain positive experiences. It is
something we need to work for and we do this by taking action and engaging in
behaviours that help us live a healthy and fulfilling life.
o Why don’t people change their behaviour? They may:
 lack knowledge and/or hold incorrect beliefs (e.g. “Vaccines cause
autism”);
 be concerned about others’ approval if they change (e.g. “My smoking
friends won’t like me if I quit”);
 lack motivation/emotional involvement (change isn’t that important to
them);
 have to many other priorities (the time isn’t right); lack belief in their
ability to successfully change their behaviour (“I’m not capable”);
 lack planning skills (don’t know how to plan change, e.g. goal-setting
skills);
 lack performative skills (don’t know how to enact change, e.g.
implementation of plans, monitoring, refusing substances);
 face difficulties overcoming existing habits and/or building new habits,
habit-breaking (give up when it gets to hard);
 live/work in an environment that facilitates current maladaptive
behaviour.
o Taking action to change behaviour therefore involves a number of processes
and skills. Many of these processes are within our control and many of these
skills can be taught. These include:
 Motivation: desire/intention to engage in behaviour
 Self-efficacy: belief in one’s ability to execute the behaviours
necessary to achieve a goal
 Goal setting: setting a defined goal that will guide behaviour
 Planning: determining how one intends to achieve their goal
 Self-monitoring: examining and recording thoughts, feelings, and/or
behaviour in relation to the goal
 Self-evaluation: assessing the extent to which one has succeeded in
reaching a set goal
 Goal review: reconsidering a goal in light of evaluation
 o Behaviour change model: There are hundreds of models out there, and this
brief schematic hits on the main points to focus on with a client. We will go
through every box of this model in the lecture. We often do not spend enough
time in the motivation stage, and so treatment can be less effective.

o Based on this model, we have some key behaviour change questions:

 How can we build confidence in achieving successful outcomes (i.e.,
self-efficacy)?
 How can we foster motivation? What are the drivers/determinants of
motivation for this particular individual and how can we
change/promote these?
 What are the properties of goals most likely to lead to action?
 How can we facilitate and optimise self-monitoring?
 What types of evaluation and feedback are most useful in maintaining
motivation and self-efficacy and optimising goal review?
o What about you? Pick a behaviour from your own life that you would like to
change to improve your wellbeing. Common examples include: reducing
alcohol intake; quitting smoking; increasing physical activity; eating healthily;
improving sleep habits; spending more quality time with family and friends;
reducing procrastination. We begin with motivation (for clinicians and
ourselves).
 Motivation: An individual’s desire/intention to engage in a behaviour. Do they want
to do it? If yes, then great! We can move on to goal setting. If no, then we need to
stop and increase motivation first. Just because a client is in the room does not mean
they are motivated to change.
o Motivation is critical to behaviour change: Motivation is pre-requisite to
behaviour change. It is a function of the extent to which we want to act in a
certain way and believe we should act in a certain way. Behaviour change is
challenging when there is conflict between what we want to do and what we
should do. For example, when what we want to do (smoke, drink, eat junk
food) is not in our best interests.
o Determinants of motivation: knowledge; attitudes; beliefs; identities and
values; self-efficacy. Motivation is based on some form of story clients have
developed for themselves that includes some or all of the above.
o The motivation “story”: For example, “I don’t know how to change, change
will be awful, my friends won’t like me if I change, this new behaviour isn’t
‘me’, I don’t have the skills to change,” compared to, “I know how to change,
change will be hard but it will feel good, my friends will still like me and if
 they don’t they weren’t true friends to begin with, this new behaviour is
consistent with my values, I have the skills to change.”
o We need to work with clients to change this story. Evidence from the
following areas of research shows that changing these determinants (of
motivation) results in increased motivation and behaviour change: smoking
cessation; alcohol; cancer screening; sun protection; exercise; diet.
o Increasing motivation:
 Knowledge: We need to ensure people are aware of (and understand!)
relevant information. What do people need to know about a new
behaviour they need to enact or old behaviour they need to stop
enacting? For example: “Taking this medication may reduce your
cholesterol by X”; “Going on a 30 minute walk every day may
improve your heart health by X%”; “Within 2 days of quitting
smoking, your sense of taste will improve”. It is very rarely knowledge
that needs changing (from lecturer’s experience). With clients with
lower levels of health literacy, it can be effective, however, most
people know smoking is bad, and that alcohol is a poison, and that diet
and exercise are important. Simple information is not enough to
change motivation in most cases. It is a determinant, but for most
population groups this is not the target.
 Attitudes: This is much more relevant. People must believe the
advantages/benefits of behaviour change outweigh the
disadvantages/costs of performing the behaviour (i.e., they hold a
positive attitude to behaviour change). For example: “It will feel good
to quit smoking/increase my physical activity”; “Taking my
medication/wearing my hearing aids/doing my rehabilitation exercises
will reduce my pain/prevent illness/increase my physical strength”. It
is about convincing people that the inconvenience is worth it. This is
really hard, and it is really important to emphasise personal relevance –
what are the benefits of change for this person? What is their story?
There is a “decisional-balance framework” (a quadrant) that helps
conceptualise pros and cons of changing vs not for that person. For
example, to motivate people to stop smoking, we leverage being able
to run around with their kids/grandkids and see them grow up. We
want to provide many arguments and repeat as needed. We also want
to provide people with substitutes or alternatives to behaviour if they
are giving something up that brings them pleasure. For example, low
fat alternatives to liked foods. This will lessen cons of changing.
 Normative beliefs: Others’ approval/liking is a powerful motivator.
Motivation will be higher if one perceives more social (normative)
pressure to perform the behaviour than not to perform the behaviour or
vice versa. For example, eating fruit and vegetables – there is more
social pressure to consume than not to consume. For example, smoking
– there is more social pressure NOT to smoke than there is to smoke,
however in an ingroup, this may be very different. We want to get to a
position where client believe: “Others will approve of me/like me more
if I quit smoking/reduce my alcohol intake/take my medication”.
Changing normative beliefs is difficult when the behaviour people
need to enact contradicts the behaviour patterns of their in-group. For
example, getting smokers to quit smoking when their family and
 friends smoke. We need to work with people to overcome these norms.
For example, when in the first few weeks of behaviour change, can
they avoid people who trigger old behaviour patterns? Can they shift
the location of social events from the pub to a café? We discuss with
client the concept of ‘enabling’ and how others benefit from the status
quo, which is of detriment to the client, e.g. a smoker in a group that
doesn’t want to be alone.
 Identities and core values: We want people to perceive performance to
be more consistent than inconsistent with self-image/their values. Core
values and identities determine priorities. We want to weaken current
wants/desires by explaining to people that what we want (the
behaviour they are engaging in) is not necessarily aligned with who we
want to be. It is about highlighting this contradiction. For example,
someone may want to be a present parent, but their alcohol intake
prevents this. We highlight this discrepancy to them. Values-based
work can help clients to identify what their values are and how their
current behaviour isn’t aligned with their values, and thus how
behaviour change may be more aligned. It gets tricky when values are
aligned with poor behaviour, and the rigid value actually generates
poor behaviour. Harris has a term for this, check out his websites on
values.
o Reflection on own behaviour (procrastination): Rate motivation to change –
6/10. 7 is the magic number Harris talks about. If motivation is less than 7, the
client won’t change. Is there extra information you need? Are the cons higher
than the pros of changing? Are you worried about what people think? What do
I do with this information?
 Self-efficacy: This is a determinant of motivation that we are separating because it is
not only a determinant, but it also impacts other areas of the model. This refers to an
individual’s belief in their ability to execute the behaviours necessary to achieve a
goal.
o Self-efficacy is also critical to behaviour change: Evidence from the following
areas of research shows that the effects of an intervention on health behaviour
are partially mediated by changes in perceived self-efficacy: smoking
cessation relapse; pain management; control of eating and weight; success of
recovery from heart attack; adherence to preventive health programs;
consistent use of contraception; exercise.
o Increasing self-efficacy: Four sources of efficacy information:
 Mastery experiences (learning through personal experience, most
potent)
 Vicarious experiences (learning that occurs through observation of
other people)
 Verbal persuasion (communication from others about one’s
capabilities, most commonly used by health professionals, probably
too much)
 Emotional regulation (people rely on information about their
physiological state/feelings to determine their capabilities, “I am
anxious therefore I am not capable).
o Mastery experiences:
 Rationale: Achieving mastery over a difficult or previously feared task
increases self-efficacy. Success builds self-efficacy and failure
 undermines it. Successive mastery leads to a refinement of skills and
the development of coping mechanisms to deal with problems.
 Approaches for practice: set challenging but achievable tasks;
encourage practice, practice, practice; gradually increase the difficulty
of tasks (graded steps); attribute accomplishments to the person’s
abilities; psychoeducation on the difference between a lapse and a
relapse, and build the self-efficacy to deal with a lapse too (a lapse is a
single event where we re-engage in goal-directed behaviour
immediately, a relapse is more continuous and takes longer to engage
in goal-directed action again). Clients will often think that making one
mistake means relapse, but this is not the case.
 Example: Increasing physical activity via a graded plan, worked on
collaboratively with the client. If it is going to work, it needs to be
gradual. The starting point depends on where the client is at, for
example, a 20-min walk might be too much for someone with chronic
pain, or not enough for someone without it.

o Vicarious experiences (observational learning):

 Rationale: Seeing others like ourselves succeed at a task can strengthen
self-efficacy. Seeing others like ourselves struggle may undermine
self-efficacy.
 Approaches for practice: We ask clients, “Do you know anybody who
has tried this behaviour change before?” E.g. Do you know anybody
who has quit smoking successfully? What did they do? How did they
do it? We encourage clients to mix with peers who have succeeded. If
they don’t know anyone personally, we encourage clients to join peer
support groups. We encourage clients to discuss with peers what they
did to succeed and how they succeeded. We encourage clients to copy
their peers. It is important to ensure that the peer/model overcame any
difficulties through determined effort, rather than with ease/luck.
o Verbal persuasion:
 Rationale: Providing credible feedback/reinforcement can boost self-
efficacy. Effectiveness of this approach is dependent on the client
believing what they’re told about their capacities.
 Approaches for clinical practice: We give clients good (i.e.
appropriate, constructive) feedback on their performance. The
feedback must be credible, so it can’t be overly positive (this is the
issue with Instagram self-help). Examples of good feedback: “Well
done, you are nearly there. Adding X to the plan might help you
achieve your goal.”; “You managed to achieve your goal every day
except Sunday. That’s a great start! Let’s chat about what happened on
Sunday to see what we can learn.”; “You did X twice this week, which
means you can do it! What can you do to make it happen more often?”;
“Your test scores show that you have great potential to quit smoking.”
o Emotional regulation:
  Rationale: Positive mood can boost self-efficacy. Anxiety/high
physiological arousal can undermine self-efficacy, especially if the
person believes that arousal impairs performance.
 Approaches for practice: We want to normalise anxiety. We reduce
stressful elements of task performance by managing mood before and
during performance. Psychoeducation can be used to teach clients
about the “anxiety wave” and how to ride it (controlled breathing,
PMR, imagery). Psychoeducation can also teach clients the Yerkes-
Dodson law (when it comes to top performance, you need a particular
level of arousal to make it happen, not too much or little): evidence
shows that optimal performance occurs when one is physiologically
aroused, which can be used to challenge client beliefs that they can’t
do something when they experience any anxiety.
o Reflection on own behaviour: Rate self-efficacy – 3/10.
 Goal setting: Defining a goal that will guide behaviour. What do you want to do?
o SMART goals – essential to behaviour change: Not all goals are created equal.
“I will work on my fitness” is very different to “I will go to the gym three
times this week and exercise for one hour on each of those occasions”. The
first goal is vague and ambiguous – When will you work on your fitness?
What does ‘working on’ your fitness mean? The second goal is clear and
unambiguous (although we could be even more specific and note which
exercises we will be doing at the gym and/or the average heart rate we would
like to maintain during our workout!). To increase chances of changing their
behaviour, developing SMART goals is vital. Clients usually come in with a
very general goal (“I want to be happy”), and then we need to work with them
to figure out what it looks like for them, and what behaviours we can put in
place. What are they doing that shows they are happy?
o SMART goals meaning:
 Specific: State exactly what you want to accomplish (e.g. who, what,
when, where, why). The goal is clear, detailed, and well-defined.
 Measurable: Can you clearly and easily demonstrate and evaluate the
extent to which the goal has been met?
 Achievable: Ensure goal is challenging but realistic, i.e. within the
client’s ability to achieve.
 Relevant: How does the goal relate to the client’s overall objective?
 Timed: Does the goal have a clear timeline?
o Once you have developed a SMART goal, you may need to develop smaller
SMART goals that build up to the bigger goal. For example, if your goal is to
be able to run 5kms in 2 months’ time, what smaller SMART goals need to be
developed to increase their chances of achieving that? This might take the
form of weekly goals that become increasingly challenging (e.g., ‘walk 3 kms
every day this week’ to ‘walk 4 kms on 5 days this week and run 500 metres
on 2 days this week’ to …). Quitting smoking can be interesting, it will never
happen straight away, we usually set a “quit date” and work towards it.
o Reflection on own behaviour: Set a SMART goal – Have one of my essays
completed the day it is due. When it comes to clinical practice, this is usually
the hardest thing. This is often due to a lack of work on motivation.
 Taking action:
o Step 1: Assessment of skills. It is important to ensure someone has the skills
required to engage in a particular behaviour before they attempt it. Attempting
 to take action and being unable to can undermine self-efficacy. Types of skills
include motor (e.g. can they do rehab exercises?), social (e.g. can they say no
to an offered cigarette?), self-regulatory (e.g. can they plan and monitor
progress?), and self-care (e.g. can they manage any anxiety that might arise?).
o Step 2: Teaching skills. If your assessment concludes that one or more skills
are lacking, the following can be used to develop these skills: instruction –
telling the client what to do/how to do it; demonstration – showing the client
what to do/how to do it (modelling); practice (most potent) – asking the client
to take action in session with role play potential scenarios or trying out the
behaviour (e.g., rehab exercises); feedback – provide feedback to client on
how they did.
o If-then planning – a key cognitive skill and tool: After SMART goals are
developed, it is time to implement the steps required to achieve those goals.
These ‘implementation intentions’ specify when, where, and how the goal will
be achieved and take the form of an ‘If-Then’ plan. IF identifies the cue to act.
This might be a time/place. THEN identifies an effective goal-directed
response. E.g. “If I find myself in X situation, then I will perform goal-
directed response Y.” It can help in 3 main ways.
 If-then planning can help your client identify situations that are usually
associated with the behaviour they are trying to change and then
specify a response that is designed to overcome their usual habits in
these situations. For example: If their goal is to lose weight or eat
healthily, a relevant if-then plan might be “If I am invited to an event
that I know will have unhealthy food, then I will make sure I eat
beforehand.”
 If-then planning can also help clients identify situations that they can
link to engagement in a new behaviour. That is, it can help them seize
opportunities/cues to act and remember these cues. For example: If
your client has been prescribed medication and needs to take this twice
per day, a relevant if-then plan might be “If I have finished brushing
my teeth, then I will take my medication”.
 If-then planning can be used to protect motivation from unhelpful
thoughts/emotional arousal (i.e., shields the goal from a problem). For
example: “If I think that change isn’t worth it/will be too hard, then I
will start the behaviour anyway/go back to my list of reasons for why I
am doing this/go back to my list of the positive outcomes of this
behaviour”; “If I am feeling anxious, then I will take a few minutes to
control my breathing”.
 See Gollwitzer and Sheeran for research about preparing people for
therapy (which can be anxiety inducing for many). Demonstrated
effectiveness of if-then plans in rates of showing up to therapy.
 If-then planning enhances goal-directed action by: facilitating cue
identification (“I’m brushing my teeth. That means it is time to take
my medication”); creating an automatic association between context
and action (increased cue detection); leading to automation of
behaviour, thus reducing effort (clients no longer need to think about
behaviour, they just do it); increasing speed of response; mimicking
the effects of previous practice (i.e., consolidation).
 Reflection: Create and if-then plan – If I’m sitting on the balcony, then
I am working on my essay for the week before it is due.
 Self-monitoring and self-evaluation: It is very important that your client monitors
their attempts at behaviour change and evaluates their progress. This is because
without monitoring and evaluation, they are “driving blind” and are unable to
determine: Whether their behaviour really is changing (i.e., whether they are
progressing toward their goal); How much their behaviour is changing (i.e., the extent
to which they are progressing); Why their behaviour might not be changing (i.e.,
reasons for lack of progress); Why their behaviour is changing (i.e., reasons for
progress); How behaviour change is making them feel (e.g., uncomfortable,
empowered). The things to self-monitor are: behaviour patterns in relation to the goal;
immediate reactions; changes in wellbeing.
o Monitoring behaviour: As a clinician, we can learn the frequency of efforts
required to resist old behaviour or instigate new ones, the perceived difficulty
of the task, and the frequency of slips (failure to act as planned). In addition,
we can learn if each of the above are declining over time, and if not, what
strategies can be put in place to speed progress? What has been the success of
strategies used to date? /monitoring behaviour requires good records of
behaviours. Digital apps and tools like “Habitica” are particularly useful here.
We make sure they take appropriate actions, like providing relevant rewards
for achievements, and taking remedial action if progress is inadequate.
o Monitoring reactions: It is about monitoring the actual experience while acting
on or resisting temptations, linking physiological responses to experiences –
“What were you feeling?” We set the challenge of noticing changes in levels
of reactions, and mindfulness techniques can help here. We want to separate
initial “automatic” reactions from those that arise due to thoughts (e.g.
expected anxiety vs catastrophising). We then want to assess reactions to slow
progress and potential diminishing self-efficacy. Behaviour change will be
slow, so we need to make sure we don’t lose clients because of this.
o Monitoring changes in aspects of well-being: We monitor changes in well-
being that might be related to the behaviour change, and this if from minutes
after the behaviour to days and weeks after, e.g. we may feel bad after saying
no to a cigarette, but then we feel fine an hour later. If wellbeing is positive
after change, then great! It shows life can be better and the feared negatives
have not occurred. If it is negative, then we need to work out whether this is
linked to the behaviour change. Is this effect temporary (it usually is), and
what can we do to minimise negatives.
o Summative evaluation: We evaluate all three areas. This should be done
regularly in the early stages, or when triggered by a crisis. We need to
celebrate successes (e.g. with rewards) and use them to build self-efficacy, as
well as learn from setbacks and have a recovery plan ready. We learn how to
view setbacks positively as teachable moments.
o Goal review: If the goal wasn’t met, we have to ask if the goal was too
ambitious, or whether it was specific enough. We amend the goal if needed. If
the goal was met, we ask if we can make the goal slightly more challenging.
We want to avoid reviews when actively facing challenges. We need to be
objective as possible and reviewing a goal when feeling deflated will colour
the judgement.
 o Reflection: Create a monitoring plan for the behaviours in which you wish to
engage.

 Making and breaking habits: So, your client is motivated to change, believes they
have the skills required to change, has developed SMART goals and if-then plans, is
monitoring their progress and revising their goals accordingly. However, they are still
finding change effortful! What’s going on? Most likely, behaviour change hasn’t
become habitual yet. Many attempts at behaviour change fail because they don’t take
the step from controlling action to doing it without thinking (e.g., they devote a lot of
effort to losing weight for an event then stop before their behaviours become
habitual). The final stage of successful behaviour change is creation of a habit – your
client doing what they wanted to do without having to set goals, plan, review, monitor
etc – they just do it! This is the ultimate goal for clinicians.
o What are habits? Habits are automatic behaviours that are often enacted
outside of our awareness.
o How are habits formed? Habits are formed via repeated matching/associations
over time between: a cue or situation and a behaviour; the behaviour and a
reward (emotional or physiological). That is, there is an ‘if’ in the
environment, we act, and we get rewarded for this action. For example, we see
the bakery, we buy and eat the croissant, and we feel good. Once these
associations are formed, the cue can prompt what we think, feel, and do.
Habits can feel really uncomfortable trying to break.
o Making and breaking habits is critical to behaviour change:
 We use these cues to make prior planning salient (e.g., the ‘If’ in ‘If
then planning’).
 We want to work with your client on ways in which they can
identify/become more aware of high-risk situations (i.e., situations
where the cue/s to act in a certain way are salient and/plentiful).
 We also work with your client on ways in which they can consciously
acknowledge that they can make new choices. This might mean that
some high-risk situations are avoided in the short-term (e.g., going to
the break room when an email is sent around saying there is cake in
there!).
 We want to highlight to your client alternatives or substitute rewards.
 We help them learn and practice new competing behaviours (e.g., what
will client do instead). It is easier to have an alternative behaviour
ready to go than to simply think “I won’t do it”.
 The aim is to consciously link effort to values-based outcomes (e.g.,
“Doing this makes me a better father”).
 We consciously link effort to beneficial outcomes (e.g., “Doing this
will reduce my risk of cancer”, “Doing this will feel good”, “Others
will like me if I quit smoking”).
o Breaking habits:
 We want to reframe potential losses as gains (e.g., “Doing this means I
will be able to chase after my kids without losing my breath”).
 We want clients to consciously rehearse self-regulatory plans (e.g.,
engaging in controlled breathing when anxious),
 We want clients to consciously focus on improving self-efficacy (e.g.,
can-do self talk – “I can run the next 500 metres”, “I can order a coffee
without a croissant”).
 We focus on likely feelings of failure (i.e., anticipated regret) if client
does not engage in a behaviour in which they planned to engage in or
does engage in a behaviour in which they did not plan to engage (“I
will feel guilty if I buy this doughnut when I didn’t plan to”, “I will
feel awful if I don’t go to the gym when I had planned to”).
 We set some absolute rules (e.g., “For the next 3 weeks I will not go to
the coffee shop with the nice pastries)
 We want clients to learn competing thoughts (e.g., “This feeling of
anxiety is normal and will pass, I need to ride it out like a wave” vs
“This feeling is awful and I can’t stand it any longer, I must smoke a
cigarette/have a drink”)
 Over time, the cue is reconceptualised and competing behaviours and
thoughts become dominant. This is slightly different with addiction.
 Help client unlearn emotional associations, which can strengthen the
impulse to act in response to cues (e.g., when walking past the bakery:
“That cake will taste delicious” vs “That cake will taste delicious for 5
minutes but then I will feel guilty for the rest of the day”)
 Seek social support (e.g., share goals with others and ask them to help).
Help your client identify those who may not want them to change (e.g.,
if your client quitting smoking means there is only one smoker left in
the group)

Lecture 7: Psychotic Disorders

 Myth: Individuals with psychotic disorders all have the same symptoms.
o Psychosis: It can refer to a variety of disorders or syndromes, or a range of
symptoms. It is a disruption in various aspects perception, thinking, feeling
and behaviour. At the disorder level it refers to a group of disorders
distinguished from one another in terms of: symptom configuration (e.g.
delusional disorders vs schizophrenia); and duration (e.g. schizophrenia vs
schizophreniform disorder). Psychotic symptoms are included in other DSM
disorders like Alzheimer’s, OCD, or substance use disorders.
o Psychotic symptoms – Abnormalities in one or more of the following
domains: Delusions; Hallucinations; Disorganised thinking (speech); Grossly
 disorganised or abnormal motor behaviour (including catatonia); Negative
symptoms
o Delusions: Fixed beliefs that are not amenable to change in light of conflicting
evidence. There are different types:
 Persecutory delusions: i.e., belief that one is going to be harmed,
harassed, and so forth by an individual, organization, or other group.
This is the most common type of delusion.
 Referential delusions: i.e., belief that certain gestures, comments,
environmental cues, and so forth are directed at oneself.
 Grandiose delusions: i.e., when an individual believes that he or she
has exceptional abilities, wealth, or fame.
 Erotomanic delusions: i.e., when an individual believes falsely that
another person is in love with him or her;
 Nihilistic delusions involve the conviction that a major catastrophe will
occur,
 Somatic delusions focus on preoccupations regarding health and organ
function.
 Delusions can be bizarre or non-bizarre. Bizarre delusions are clearly
improbable and not comprehensible to people in that culture, e.g. an
alien has removed one’s organs and replaced them with clock
mechanisms. Non-bizarre delusions are not completely implausible, it
can’t be absolutely ruled out, but the weight of evidence is against it,
e.g. the Federal Police have a client under surveillance. Delusions that
express a loss of control of the mind or body are usually bizarre
delusions, e.g. thought withdrawal, thought insertion, thought
broadcasting.
 The distinction between a delusion and a strongly-held belief is
sometimes a bit blurry. The degree of conviction that the individual has
in the belief may determine whether we are looking at a true delusion
or a lower-grade delusional thought process.
 We can distinguish delusions as primary and secondary delusions
(older distinction). Primary delusions are those formed without any
prior event or psychopathology. Secondary delusions are those that are
theoretically secondary to some other change in the person’s
psychopathology.
o Hallucinations: Perception-like experiences that occur without an external
stimulus. Auditory hallucinations are most common, but they may occur in
any sensory modality. Hallucinations may be a normal part of religious
experience in certain cultural contexts. These experiences are often not under a
clients’ voluntary control. Hallucinations while people are falling asleep or
waking up are not included as clinically significant. Many people experience
hallucinations that are not distressing, and this also impacts clinical
significance. Note that we can diagnose someone, but this does not mean we
have to treat.
o Disorganised thinking/speech – also referred to as Formal Thought Disorder, it
is typically inferred from the individual’s speech:
 Clanging - speech pattern based on phonological association rather
than semantic or syntactic.
 Circumstantiality/Tangentiality – Speech including unnecessary or
irrelevant detail. Goal is eventually reached.
  Flight of ideas - Sequence of loosely associated concepts are
articulated. Sometimes rapidly changing from topic to topic.
 Derailment - speech train steers off-topic to unrelated things.
 Incoherence - word salad. Incomprehensible speech.
 Pressure of speech - excessive spontaneous speech production and
rapid rate. Difficult to interrupt.
o Grossly disorganized or abnormal motor behaviour: May manifest in a variety
of ways, ranging from childlike “silliness” to unpredictable agitation.
Catatonia is a marked decrease in reactivity to the environment, which used to
be quite common but is now not as much due to earlier preventative treatment.
o Negative symptoms: Diminishments of different types of behaviours. This has
some overlap with depression symptoms, so we’re looking at the combination
of all these things plus context (history, trauma, culture).
 Diminished emotional expression: reductions in the expression of
emotions in the face, eye contact, intonation of speech (prosody), and
movements of the hand, head, and face that normally give an
emotional emphasis to speech.
 Avolition: a decrease in motivated self-initiated purposeful activities
 Alogia: manifested by diminished speech output
 Anhedonia: decreased ability to experience pleasure from positive
stimuli or a degradation in the recollection of pleasure previously
experienced
 Asociality: the apparent lack of interest in social interactions and may
be associated with avolition, but it can also be a manifestation of
limited opportunities for social interactions.
 Myth: You are either psychotic or not
o Experience of psychotic symptoms in the general population (Linscott & van
Os, 2012). Psychotic symptoms (hallucinations and delusions) are present (at
various degrees of severity): These symptoms lie on a continuum in the
general population.
 In about 5% of the general population who are not seeking help;
 In about 25% of people with (non-psychotic) common mental
disorders, such as anxiety and depression;
 In around 80% of patients with psychotic disorders
 Highest prevalence in children (17%)
 Moderately high prevalence in adolescence (7%) (Kelleher et al.,
2012).
 Lowest prevalence in later adulthood (≥ 70 years) of 3% (Yates et al.,
2021).
o Prevalence of hallucinations with age (Yates et al., 2021): In all age groups,
the experience of hallucination was associated with increased risk of mental
disorder, suicidal ideation and attempts. We can infer higher risk from these
symptoms. IT is thought that brain maturation processes may account for this.
Also thought that the development of skills in emotional regulation in
 adulthood can be a factor from a psychosocial perspective.

o Hearing Voices Network: Perhaps a cold clinical approach is not always best.
About acceptance that hearing voices (and related experiences) are valid
human experiences. We want to foster respect for each person’s framework of
understanding and beliefs about their experiences. We create safe spaces for
people to go to and share experiences, and network for deeper connection. It is
about building belief in each person’s resilience and capacity to take control of
their experiences and recover. We work collaboratively and inclusively with
other services to develop knowledge and use holistic approaches to recovery.
The aim is fostering and supporting self-determination and self-empowerment.
Based on work by Romme and Escher (1993, 1996).
 DSM-5 Schizophrenia Spectrum and other Psychotic Disorders: We recognise some
people experiencing these symptoms have severely impaired functioning which
causes significant distress, and this means their experience warrants treatment. We
have structures for diagnosing various psychotic disorders.
o Brief psychotic disorder: Someone experience psychotic symptoms for a very
short period of time. Criteria is abbreviated.
 A. Presence of one (or more) of the following symptoms. At least one
of these must be (1), (2), or (3): Delusions; Hallucinations;
Disorganized speech (e.g., frequent derailment or incoherence);
Grossly disorganized or catatonic behavior. (Negative symptoms don’t
get a look in).
 B. Duration of an episode of the disturbance is at least 1 day but less
than 1 month, with eventual full return to premorbid level of
functioning.
 C. The disturbance is not better explained by major depressive or
bipolar disorder with psychotic features or another psychotic disorder
such as schizophrenia or catatonia, and is not attributable to the
physiological effects of a substance (e.g., a drug of abuse, a
medication) or another medical condition.
 Specify if: With marked stressor(s) (brief reactive psychosis) – If
symptoms occur in response to events that, singly or together, would
be markedly stressful to almost anyone in similar circumstances in the
individual’s culture. Without marked stressor(s) – If symptoms do not
 occur in response to events that, singly or together, would be markedly
stressful to almost anyone in similar circumstances in the individual’s
culture. With postpartum onset – If onset is during pregnancy or within
4 weeks postpartum.
o Delusional disorder:
 A. The presence of one (or more) delusions with a duration of 1 month
or longer. (Purely based on delusions).
 B. Criterion A for schizophrenia has never been met.
 C. Apart from the impact of the delusion(s) or its ramifications,
functioning is not markedly impaired, and behaviour is not obviously
bizarre or odd.
 D. If manic or major depressive episodes have occurred, these have
been brief relative to the duration of the delusional periods.
 E. The disturbance is not attributable to the physiological effects of a
substance or another medical condition and is not better explained by
another mental disorder, such as body dysmorphic disorder or
obsessive-compulsive disorder.
o Schizophreniform disorder:
 A. Two (or more) of the following, each present for a significant
portion of time during a 1-month period (or less if successfully
treated). At least one of these must be (1), (2), or (3): Delusions;
Hallucinations; Disorganized speech (e.g., frequent derailment or
incoherence); Grossly disorganized or catatonic behaviour; Negative
symptoms (i.e., diminished emotional expression or avolition).
 B. An episode of the disorder lasts at least 1 month but less than 6
months. When the diagnosis must be made without waiting for
recovery, it should be qualified as “provisional.”
o Schizophrenia:
 A. Two (or more) of the following, each present for a significant
portion of time during a 1-month period (or less if successfully
treated). At least one of these must be (1), (2), or (3): Delusions;
Hallucinations; Disorganized speech (e.g., frequent derailment or
incoherence); Grossly disorganized or catatonic behaviour; Negative
symptoms (i.e., diminished emotional expression or avolition).
 B. For a significant portion of the time since the onset of the
disturbance, level of functioning in one or more major areas, such as
work, interpersonal relations, or self-care, is markedly below the level
achieved prior to the onset (or when the onset is in childhood or
adolescence, there is failure to achieve expected level of interpersonal,
academic, or occupational functioning). (This is not in
schizophreniform disorder).
 C. Continuous signs of the disturbance persist for at least 6 months.
 D. The disturbance is not attributable to the physiological effects of a
substance or another medical condition.
o Schizoaffective disorder:
 A. An uninterrupted period of illness during which there is a major
mood episode (major depressive or manic) concurrent with Criterion A
of schizophrenia.
  B. Delusions or hallucinations for 2 or more weeks in the absence of a
major mood episode (depressive or manic) during the lifetime duration
of the illness.
 C. Symptoms that meet criteria for a major mood episode are present
for the majority of the total duration of the active and residual portions
of the illness.
 D. The disturbance is not attributable to the effects of a substance (e.g.,
a drug of abuse, a medication) or another medical condition.
o Others in DSM-5:
 Substance/medication induced psychotic disorder
 Psychotic disorder due to another medical condition
 Catatonia: Catatonia associated With Another Mental Disorder;
Catatonic Disorder Due to Another Medical Condition; Unspecified
Catatonia; Other Specified Schizophrenia Spectrum and Other
Psychotic Disorder; Unspecified Schizophrenia Spectrum and Other
Psychotic Disorder
o Cheat table:

o Age of onset (Sham et al., 1994):

o Epidemiology:
 Lifetime prevalence of schizophrenia: 1-2%; delusional disorder 0.2%;
schizoaffective disorder: ~0.3%
  Cross-cultural, cross-country and intra country variation: Higher
prevalence amongst migrants, developing countries and 2-fold risk
urban vs rural dwellers (McGrath, 2006)
 Schizophrenia: 3:2 male:female ratio (McGrath, 2007)
 Peak age of onset: late adolescence/early adulthood.
o Associated features:
 Depression
 Suicide (5-10% of people diagnosed with schizophrenia commit
suicide: Palmer et al., 2005)
 Anxiety
 PTSD- trauma may be the experience of psychosis itself OR associated
with treatment
 Substance use problems (may be causally related or coping
mechanism). We determine this based on the history of the client.
Sometimes hospitalization is used to test the effect of not having the
substance.
 Poor quality of life in general- occupational, relationship, social and
emotional functioning
 Stigma
 Myth: People with psychotic disorders are dangerous, unpredictable and out of
control.
o Psychosis and violence: The risk of perpetrating violent outcomes is increased
in individuals with schizophrenia spectrum disorders compared with
community control individuals (Whiting et al., 2021). However, most
individuals experiencing psychosis are not violent and do not display
aggressive or dangerous behaviour (less than 1 in 20 in women and 1 in 4 in
men, low risk). The origins of violence/aggression AND psychosis are
heterogenous- but factors that may increase risk of violence/aggressive
behaviour by individuals with psychotic disorders include: Past history of
violence*; Substance use*; Certain personality traits*; Paranoid beliefs (can
have heightened risk); Social circumstances*; Being male*; Content of
auditory hallucinations; Being young*. *also increases chance of future
violence in people without psychotic disorders. Not that this is associational,
not causal. In fact, clients are more likely to be victims of violence. The risk of
an individual with a psychotic disorder becoming a victims of violence in the
community, is up to 14 times the rate of being victimized compared with being
arrested as a perpetrator (Swanson et al., 2006). Yet, the majority of studies
focussing on violence and severe mental illness focus on perpetration of
violence- not on people with SMI being victims (Choe et al., 2008). Similarly,
a study of the British news media found that stories of violence by people with
schizophrenia outweighed news stories that were more sympathetic about the
disorder by about 4 to 1. One reason for this may be the historical
conceptualisation of these illnesses.
o Historical conceptualisations of “schizophrenia”:
 We know that in ancient texts there are descriptions of schizophrenia
like symptoms throughout history (hearing voices, odd behaviour).
This is not new. We start getting a more clinical lens in the 1800s.
 Benedict Augustine Morel (1860) proposed “demence prcoce”: This
was the first attempt at a rigorous description of what we now know as
schizophrenia. This was based on observations of individuals
 displaying a set of symptoms (common between them) and experience
early onset and deteriorating course.
 Emil Kraeplin (1989) proposed “dementia praecox”: This was a
refined more formal definition, which emphasised early onset and
deteriorating unremitting (once diagnosed it is permanent) course. His
writing is still influential in the field. It is differentiated from manic-
depressive psychosis, bipolar and other psychotic illnesses based on
clusters of symptoms, onset, course and outcome. He made some of the
initial groupings that we still use. Symptoms emphasised were
hallucinations, delusions, negativism, attentional difficulties,
stereotypies, and emotional dysfunction.
 Eugen Bleuler (1911) first coined “schizophrenia”: Conceptualised
manic depression and schizophrenia lying on a continuum. He
proposed that there is not necessarily early onset and deteriorating
course. He was ‘Breaking of associative threads’ loosening of
connections between thought structures seen as the core of the
disorder. He proposed 5 primary symptoms - Five ‘A’s’: Disturbances
in thinking; Disturbances in affect; Ambivalence; Autism (different
from contemporary, separation from society); Avolition. This was
picked up and expanded in the US by others. Carl Jung was Bleuler’s
right hand in a hospital in Sweden. Jung took on the thread of writing
about this, and his students spread far and wide.
 Kurt Schneider (1959): Proposed “first rank symptoms” of core
symptoms of schizophrenia. These are: Hearing one’s voice out loud;
Hallucinatory voices talking about him or her; Hallucinations in the
form of a running commentary; Somatic hallucinations produced by
external agencies; Thought withdrawal; Thought insertion; Thought
broadcasting; Delusional perception (ideas of reference); Made
feelings; Made actions; Made impulses. The experience of any one of
these was enough to diagnose.
 In the 1970s, it became apparent that we were not talking about the
same thing in all this literature. The US-UK Cross-National Project
(1972) and WHO Multi-Centre Collaborative Study (1974) looked at
varying rates of schizophrenia between countries due to a lack of
standardised criteria. It was found people are not describing the same
symptoms in different places. To solve this, in the late 1970s there was
development of the Feighner criteria (focused on 14 different
disorders, note homosexuality was included) and Research Diagnostic
Criteria – precursors to the landmark and expansive DSM-III. These
are more rigorous and designed to be universal. It was essentially a
group of white men from the US making these decisions, that had a
huge impact on the course of clinical psychology around the world.
 1980 the DSM-III diagnostic criteria for schizophrenia is published: It
is a narrow (neo-Kraeplinian) view with exclusion and inclusion rules
and duration criteria. Importantly it includes a criteria that the
condition must interfere with life domain functioning. It is in the DSM-
III where we see schizophrenia for the first time described in the way
we recognise it today, very much based on Kraeplin’s work. Five
subtypes are established: paranoid, disorganised (hebephrenia),
catatonia, undifferentiated, and residual. There have been some
 revisions since, but not a huge amount. The DSM-III is very much a
watershed document, diagnosis has kept to this paradigm. Interestingly
Kraeplin’s ideas didn’t gain much traction because Freud really swept
the field (this is why CBT is a thing).
 McGorry (late 1980s-present): It became apparent that Kraeplin and
Bleuler’s work reflects the system at the time (asylums), where
treatment was basically non-existent. He began to question the over-
focus on chronic samples who are only representative of very poor
outcome patients and are contaminated by institutionalisation,
medication side-effects, etc. They emphasised a need to prospectively
study first-episode patients and prodromal patients. They pointed out
that diagnosis is not stable in first episode.
 Richard Bentall (1990s – present): Bentall called for the need to study
psychotic symptoms individually, not schizophrenia as a construct. HE
really proposes throwing the book out the window. He can be very
controversial at times.
 Myth: That psychoses are purely genetic disorders.
o It is true that there is some risk associated with genes, showed by Kahn et al.,
2015 (focuses on schizophrenia): The fact that even in monozygotic twins the
risk is only 50% suggests that environment is very important. Studies where
twins are separated by adoption supports this fact.

o Psychosis and genetics is not a simple picture. There are at least 100 genes
involved (Schizophrenia Working Group of the Psychiatric Genomics
Consortium, 2014- published in Nature). This suggests we need to take an
epigenetic approach, looking at gene-environment interactions (possessing
certain genes may increase risk but only with certain environmental
conditions). This has borne the most fruit in research into the COMT gene
(breaks down dopamine and other neurotransmitters) and its interaction with
cannabis. Caspi et al. (2005) found that people with a specific form of the
COMT gene, their risk of getting schizophrenia was significantly greater. This
is a clearly demonstrated gene-environment interaction, and this is an
emerging field. So, what else might be at play?
 Myth: Psychotic disorders are caused by a character flaw.
o Biological factors:
 Neurotransmitters: The dopamine hypothesis posits that schizophrenia
may be caused by excessive dopamine function in the CNS (see figure,

hypothesis around receptor sensitivity). This was based on the

observation that drugs reducing dopamine activity also reduced the
experience of delusions and hallucinations, drugs increasing dopamine
have the opposite effect. However, there is no evidence of excessively
high levels of dopamine in the brains of schizophrenic patients. A lot
of this research focuses purely on hallucinations and delusions. Other
neurotransmitters that are proposed to play a role are norepinephrine
(noradrenaline) and serotonin.
 Brain structure: Lots of money spent on brain scans with little
outcomes, according to lecturer. People who have schizophrenia on
average have enlarged ventricles, which indicated a potential loss of
brain tissue (see figure). We also know that on average people with
schizophrenia have reduced grey and white matter, particularly in the
prefrontal cortex. This is particularly associated with negative
symptoms and poorer outcome. There have also been a number of
studies focusing on the hippocampus, which document reduced
hippocampal volume as the duration of illness increases. Normal brains
had a higher hippocampal volume than people at risk, who had higher
volume than people with first episode psychosis, which was higher
than those with chronic schizophrenia. It seems there may be some
areas of the brain potentially impacted by schizophrenia, however,
these differences that we are describing and not consistent and are
fairly subtle, and cannot be used for diagnosis (standard deviations are
huge in controls and patients).
 Brain function: Below is a scan of a person diagnosed with
schizophrenia with auditory hallucinations, and it shows the parts of
the brain that are activated during a hallucination. This suggests that it
 may not be about structure and volume, but instead about brain

function.
o Neurocognition in schizophrenia – the following difference have been found
between healthy controls and schizophrenia patients: deficits in sustained
auditory and visual attention; problematic initial processing of information
into sensory memory; impaired detection of relevant stimuli that are embedded
in irrelevant “noise”; problematic organisation of information in working
memory; diminished executive function; language – thought disorders;
cognitive set changing (switching); deteriorated IQ; diminished psychomotor
speed. Note that none of these can be diagnostic because the standard
deviations are too high. They are trends suggesting differences.
o Social cognition (how we think about others): This area has the most robust
evidence. People with psychosis do more poorly on tests of social cognition
that healthy people. This deficit (again not diagnostic) may influence or be
associated with the extent of impact on general functioning. Emotion
perception, which is the ability to comprehend emotional cues in a social
context, is impaired. So too is social perception, which is the ability to
comprehend communicative cues in a social context (may not be emotional).
o Psychological factors: A lot of these are more recent, and are just being looked
into now.
 The schizophrenogenic mother was proposed early by Fromm-
Reichmann (1948). Proposed that cold, aloof, overprotective,
domineering mothers strips the child of self-esteem and stifles
independence. This was thought to increase risk. There is particular
risk if the father is passive. This was wholly discredited by Hirsch and
Leff (1975).
 Social factors: More recently research has gone into this area. Living in
an urban environment, migration, and being socially excluded
increases risk for a schizophrenia diagnosis. Do some environments
make you psychotic? Van Os conducted a study that suggested yes,
especially if you are a member of a minority group in high density
living and more so if you use cannabis.
 This research has translated into the development of the social defeat
hypothesis: This proposes that the negative experience of being
excluded from the majority group increases the risk of psychosis by
sensitizing the mesolimbic dopamine system and thereby to an
increased risk of schizophrenia or psychosis (Selten and Cantor-Graae,
2005; Selten et al., 2016). There is lots of supportive evidence: the
protective effect of high ethnic density, i.e. residence in a
 neighbourhood where the own ethnic group is well-represented
(Schofield et al., 2017); experiments with rodents that demonstrate
dopamine sensitization in defeated animals (Hammels et al., 2015); a
positron emission tomography (PET) study showing increased
dopamine synthesis and increased stress-induced dopamine release in
the striatum of individuals (healthy volunteers, clinical high-risk
subjects and schizophrenia patients) with a personal or parental history
of migration (Egerton et al., 2017); the pattern of findings in Israel (i.e.
a modest increase in risk among first generation non-black migrants
and the absence of an increase in risk among second-generation
migrants) may fit with this interpretation, because the migration of
Jews to a Jewish state involves a change from social exclusion to
inclusion. This kind of idea is still very new, but is a very attractive
hypothesis.
 Childhood trauma: A large body of literature suggests a significant
proportion of people with psychotic disorders report traumatic
experiences in childhood, such as sexual and physical abuse.
Numerous population based studies suggest that childhood trauma is
an important risk factor for psychosis- a history of abuse was related to
psychotic symptoms and/or the diagnosis of a psychotic disorder either
during adolescence or adulthood (e.g Lataster et al., 2006; Spauwen et
al., 2006; Kelleher et al., 2008; Arseneault et al., 2011; Janssen et al.,
2004; Shevlin et al., 2007; Cutajar et al., 2010; Bebbington et al., 2004,
2011; Whitfield et al., 2005). John Read, Richard Bentall, Tony
Morrison are all outspoken in criticising mainstream
psychiatry/psychology for ignoring role of childhood sexual abuse in
the development of psychosis.
 Potential psychological mechanisms of childhood trauma: Cross-
sectional studies have demonstrated that negative perceptions of the
self, anxiety, and depression partially mediated associations between
trauma and psychotic symptoms- suggesting strong relationships
between negative personal evaluations and low self-esteem, negative
affect, and the characteristics of positive symptoms. Lardinois et al
(2011) found a significant, interaction between daily life stress and
childhood trauma on both negative affect, and intensity of symptoms in
patients with psychosis, suggesting that, a history of childhood trauma
is associated with increased sensitivity to stress.
 Potential biological mechanisms of childhood trauma: reduced cortical
thickness and dysregulated cortisol following exposure to childhood
trauma may facilitate development of psychosis. Gene-environment
interactions are likely to play a role- Alemany et al (2011) found that
the relationship between childhood abuse and psychosis was
moderated by the BDNF-Va166Met polymorphism, with Met carriers
reporting more positive psychotic-like experiences when exposed to
childhood abuse than did individuals carrying the Val/Val genotype.
 Stress: A stress-vulnerability model has been factored in to talking
about etiological pathways for psychosis. This is often explained to
clients to help them conceptualise trauma. The relationship between
stress and coping mechanisms (potentially poor) has been implicated in
the development of psychosis. This is not an empirically demonstrated
 model, but it can be helpful in reducing self-blame by putting
experiences in a broader context. It facilitates conversations around
coping as well.

 Cognitive factors: People like Morrison, Bentall, Birchwood and

Garety have proposed cognitive-behavioural models for working with
people with psychosis. The core of the model involves culturally
unacceptable interpretations of “intrusions into awareness” (thoughts,
feelings or images intruding on our consciousness without our control).
Most of us can dismiss these intrusions, however someone with
psychosis may not be able to do this. The role of the patient’s appraisal
of intrusions is central. According to this model, culturally
unacceptable interpretation results from a faulty knowledge of self
(and other factors), which leads to a misattribution of thought to an
external source. There is a paper (Morrison, 2001) describing this
model. Below is taken from the paper, with a plain language version
and example also attached. This echoes Beck’s model for anxiety and
depression. This also provides avenues for treatment.
o Substance use and psychosis: Substance-induced psychosis can be short-term,
during intoxication or withdrawal, i.e. amphetamines, cocaine, hallucinogens.
However, these psychotic symptoms can play a role in the development of
longer term psychotic experiences. The drug that has been looked at the most
is cannabis and its role in psychosis.
 Swedish conscript study: Andreasson et al. (1987) found that those
who had used cannabis by 18 years were 2.4 times more likely to
develop schizophrenia than those who had not, in comparison with
those who had not used cannabis by 18 years. This was one of the first
of its kind, and was a massive study, following people up over 15
years. There were a number of problems with this study (e.g. did not
take into account other drugs).

 Because of these problems, Zamit et al. (2002) conducted a follow-up

study, which reported on a 27-year follow-up on the original study’s
cohort. The relationship between cannabis use and schizophrenia
persisted when controlling for other factors such as other drug use,
psychiatric symptoms at baseline. It was estimated that the attributable
risk of cannabis use to schizophrenia was 13%. There have since been
well-developed studies that support this finding.
  Christchurch Health and Development Study: Daily cannabis users had
rates of psychotic symptoms that were between 1.6 and 1.8 times
higher (depending on factors controlled for).
 Netherlands Mental Health Survey and Incidence Study: 17 times more
likely to report clinically significant psychotic symptoms
 Epidemiological Catchment Area (ECA) Study: daily cannabis use can
double the risk of experiencing symptoms of psychosis.
 Cohort studies in context:

 Schoeler et al. (2016), most recent study: On cannabis use and risk of
relapse. Prospective cohort study followed up for at least 2 years after
the onset of psychosis 220 patients who presented to psychiatric
services in South London, England with first-episode psychosis.
Change in cannabis use status (eg, from user to nonuser) and change in
pattern of continued cannabis use within the first 2 years after onset are
risk factors for relapse. These associations were independent of the
effects of other potential confounders that vary over time, such as
medication adherence and other illicit drug use. The longer the period
of continued [monthly] cannabis use after onset of psychosis, the more
likely a patient is to experience a relapse. Cannabis use status and
pattern of continued cannabis use after onset of psychosis are
predictive of subsequent relapse but not vice versa. There is certainly
something going on that we need to understand better.
 Myth: People with psychotic disorders cannot lead productive lives.
o We know this is false, and the outcome of schizophrenia is highly variable.
We don’t fully understand what influences this outcome. Outcome can also be
defined in various ways. Historically it is defined in terms of symptoms, and
treatment aims to reduce these experiences. Whilst this remains an aim,
services have often shifted to looking at other aspects of outcome that are not
just clinical, looking at functional outcome or quality of life outcomes. We
may not stop symptoms, but this is not all we should focus on.
o Illness course: We know recurrence is very common, and that most people
who have a psychotic episode will have more than one. Note the piece on the
graph showing good recovery. Outcome is not as pessimistic as has been
 depicted.

o Relapse rates: Up to 80% of First Episode Psychosis patients will experience a

psychotic relapse within 5 years of remission from the initial episode
(Wiersma et al., 1998; Robinson et al., 1999). An EPPIC 7 year follow-up
study (FEP) found: symptomatic remission 37-59% cohort; social/vocational
recovery 31%; ~25% both social/vocational recovery and symptom remission
(Henry et al., 2010).
o Risk factors for relapse: Risk increases with substance use, medication non-
adherence, carer critical comments, poor premorbid adjustment showed a
consistently positive association with relapse. Factors that do not increase risk
of relapse include duration under illness, duration under psychosis,
positive/negative affective symptoms, age of onset, insight, gender, marital
status, education and employment (Alvarez-Jiminez et al., 2012). We are
starting to better understand why some people relapse and some don’t.
o Expressed emotion (EE): Brown 1950’s and 60’s noticed many relapsing
patients shared common family environments characterized by conflict,
criticism, hostility, over-involvement. He developed the Camberwell Family
Interview to assess patterns of family interaction. Relapse at 9 months and 2
years associated with: high EE; more than 35 hours face-to-face contact with
 high EE family; not taking neuroleptics.

o We are interested in relapse because we know that the longer people are
unwell, the less favourable the outcomes are. The impact of relapse/chronic
illness can involve unemployment, housing difficulties, poor physical health,
side-effects of anti-psychotic medication, and even premature death (Hjorthoj
et al., 2017).
 Myth: Psychotic disorders are untreatable, and all sufferers need to be hospitalised.
o Psychosis and hospitalisation:

o Psychosis and treatment: Pharmacological treatment is the primary approach

in acute phase of illness. The best practice is a low-dose approach. Evidence
shows that “atypical anti-psychotics” have fewer side effects than “typicals”.
The Soteria model was proposed by Bola and Mosher (2003), which advocates
for highly supportive care, usually medication free, living in a community.
This has shown comparable results to treatment as usual.
 Myth: Psychologists do not have role in treatment of psychotic disorders. Certain
psychological treatments for psychosis have been shown to be effective. CBT seems
to work for addressing hallucinations, delusions and negative symptoms. Substance
 use, family education, psychoeducation of patient, relapse prevention, and
occupational and social functioning are also shown to be effective.
 Psychotic disorders: current issues and debate
o Ongoing issues: There are no biological markers or physiological tests to
diagnose schizophrenia. The aetiology continues to be uncertain. There is
ongoing debate about whether schizophrenia is a valid diagnosis. See the
entire issue of Schizophrenia Research (Vol 242, 2022).
o Prevention: The field has moved to thinking about prevention in people at risk
of developing psychosis.

o Culture: Study by Westerman (2021). Looked at descriptions of Aboriginal

people experiencing “visits” from loved ones following their passing as a
normal aspect of grieving. Can be associated with ‘being sung’- non-physical
retribution for wrongdoing (payback) involving conjuring (or calling/
ceremonial singing for) spirits to inhabit the person’s psyche and for bad
mental, physical, or spiritual health to result. Often associated with little
distress or agitation- cf psychosis which is often accompanied by agitation
and/or distress. Visits and ‘being sung’ is a separation of “self” from the
“entity” –“I am being sung by, or I am being visited by” cf “I am god, I am the
devil”. The content of hallucinations in the context of visits or being sung are
consistently of a cultural nature – visually it may be spirits being seen or when
voices are heard these will be from “cultural beings” or take on a consistently
cultural form. We cannot automatically assume symptoms are inherently
negative, particularly given cultural differences.
o Stigma: Schizophrenia has a long history of neglect, demonisation and
concealment. Numerous studies have demonstrated that schizophrenia is less
recognised by general public than other disorders such as depression. The
myths highlighted in lecture are damaging to individuals with schizophrenia
because they maintain a culture and environment that heightens risk of
prejudice and discrimination- thereby limiting opportunities for recovery and
increasing stress.

Prac 3

 Psychosis:
o Can refer to a variety of disorders or syndromes, or a range of symptoms.
o At the disorder level it refers to a group of disorders distinguished from one
another in terms of: symptom configuration (e.g. delusional disorder vs
schizophrenia); and duration (e.g. schizophrenia vs schizophreniform disorder)
o Psychotic symptoms – Abnormalities in one or more of the following
domains: delusions; hallucinations; disorganised thinking (speech); grossly
disorganised or abnormal motor behaviour (including catatonia); negative
symptoms.
o Delusions: Fixed beliefs that are not amenable to change in light of conflicting
evidence.
o Hallucinations: perception-like experiences that occur without an external
stimulus; auditory is most common but may occur in any sensory modality;
hallucinations may be a normal part of religious experience in certain cultural
contexts.
o Other cognitive and behavioural symptoms: disorganised thinking/speech;
grossly disorganised or abnormal motor behaviour; negative symptoms.
o DSM-5 Schizophrenia: Two of more of: Delusions; Hallucinations;
Disorganized speech; Disorganized or catatonic behavior; Negative symptoms.
Markedly reduced personal, academic or occupational functioning Persists for
at least 6 mos. Not due to other psychological illness, substance use, or
medical condition.
o Changing minds – an inside story: What a horrible video.
o Schizophrenia Mnemonic: S CHaND (Speech disorganised, Catatonia,
Hallucinations, Negative symptoms, Delusions).
o What is a hallucination? Origin (Latin): Hallucinatio – to wander mentally or
to be absent in mind. Hallucinations have historically been defined as an
aberrant perception – a perceptual event in the complete absence of an
environmental stimulus. But, are you ever in the complete absence of
environmental stimuli? (unless sensory system dysfunction as in Charles
Bonnet Syndrome). Perhaps a more comprehensive definition might be ‘a
perceptual event in the absence of a corresponding environmental stimulus’.
The experience occurs when awake, resembles veridical perception, and is not
under conscious control. Hallucinations can be experienced in any sensory
modality. The most common hallucination in mental disorder is the auditory-
verbal type (hearing voices). Before scientific explanations were provided,
hallucinations were considered to be messages from god, angels, demons, or
integral parts of spiritual ceremony. For example: Joan of Arc (Saint Michael
and more); Moses (god); Witches; Native American ceremony (Ayahuasca or
peyote).
o Non-clinical hallucinations tend to: be more subtle than hallucination in
clinical populations; be more positive, less distressing, less frequent, lesser
impact on function; be associated with better insight into their occurrence;
occur in all sensory modalities; be common on boundaries of sleep, during
hypnogogic and hypnopompic states; vary as a function of various factors,
including personality types and traits: e.g. schizotypal and hypomania. This
makes sense, as these are thought to related to the experience of schizophrenia
and bipolar disorder, respectively.
o Cognitive model of psychosis: Need to read to whole paper to fully understand
the model
  E.g.:

o The last video is so amazing. She is so articulate it’s crazy.

Lecture 8: OCD and Related Disorders

 DSM- 5 Obsessive-Compulsive and related Disorders:

o Obsessive-Compulsive Disorder
o Body Dysmorphic Disorder
o Hoarding Disorder
o Trichotillomania (Hair-pulling disorder)
o Excoriation (skin-picking disorder)
o Substance/Medication-induced Obsessive-Compulsive and Related Disorder
o Obsessive-Compulsive and Related Disorder Due to Another Medical
Condition
o Other Specified Obsessive-Compulsive and Related Disorder
o Unspecified Obsessive-Compulsive and Related Disorder
 Obsessive-Compulsive Disorder: Used to be considered and Anxiety Disorder
(separate from things like BDD) but is now part of a new category entirely which
links these disorders with others.
o Diagnostic criteria (distilled):
 A. The experience of obsessions, compulsions or both;
 B. These experiences cause marked distress, are time consuming (>1
hr/day) or significantly interfere with functioning and relationships.
 Specify if: Good/fair insight; Poor insight; Absent insight/delusional
beliefs
o Obsessions: Refers to persistent ideas, thoughts, impulses, or images that are
experienced as intrusive and inappropriate and cause marked anxiety or
distress. An individual may recognize these experiences as products of their
own mind and are thus differentiated from delusions. Common types of
obsession include: fears of contamination; repeated doubts (safety, scruples,
e.g. “did I shut the front door? Need to check”); need to have things in a
 particular order; sexual, horrific or blasphemous imagery (may be ego
dystonic, e.g. parent harming their child); aggressive or inappropriate
impulses; nonsensical thoughts or images.
o Compulsions: Repetitive behaviour (e.g. handwashing, checking) or mental
acts (e.g. praying, counting, repeating words silently), the goal of which is to
prevent or reduce anxiety. This can include rigid/stereotyped acts according to
elaborate rules without any real explanation of them. The most common types
of compulsions include: washing and cleaning; checking; repeating; ordering;
mental rituals (e.g. counting, prayers); reassurance seeking; compulsive
shopping.
o Rates of symptoms in general population: Up to 80% of the population may
experience intrusive, unpleasant, unwanted thoughts. More than 50% of the
population may engage in ritualised behaviour (Crino et al., 2005).
o Prevalence of OCD symptom dimensions (Fullana et al., 2010):
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o Epidemiology of OCD: Has 12-month prevalence of 1.2% and lifetime
prevalence of 2.3% (US data, Ruscio et al., 2010). There is no difference in
prevalence between male and female adults. The average age of onset is 19
years, but childhood onset and later age onset are not unheard of. The is no
difference between OCD and non-OCD in gender, marital status, education,
migration status, urbanicity. It usually has a fluctuating course, often waking
and waning in conjunction with stress levels. There is a chronic course in
approximately 50% of cases.
o Childhood onset OCD: Between 1/3 and ½ of adult patients report that they
first developed OCD during childhood, so it is not uncommon. However, it is
also not uncommon for children to engage in ritualised behaviour, so it is often
about determining why some people continue these behaviours and some
don’t. Childhood onset OCD may be more common in boys than in girls
(Geller et al., 1998; Geller, Biederman, Faraone, Bellordre et al.,
2001; Swedo, Rapoport, Leonard, Lenane, & Cheslow, 1989; Tükel et al.,
2005; Zohar et al., 1997). Why the fuck did I need so many references for that.
Looks a bit OCD.
o Common symptoms profiles: 90% of patients with OCD have obsessions and
compulsions. 8-20% have obsessions and mental rituals, but not behavioural
compulsions.
o OCD is a term used a bit loosely in the population, and this somewhat
disenfranchises those who truly meet criteria for this disorder. This is a hugely
distressing and isolating experience.

o OCD and gender (symptoms) (Torresan et al., 2013):

18
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o OCD comorbidity: MDD (28.4%); Obsessive Compulsive Personality
Disorder (OCPD)(24.5%); GAD (19.3%); Specific Phobia (19.2%); Social
Phobia (18.5%); suicidal ideation within the last month (6.4%); lifetime
history of suicide attempt (9.0%) (Brakoulias et al., 2017).
o Causes of OCD: Lots of different hypotheses and we don’t fully know. In
some cases it may be associated with early childhood experience and critical
learned responses (similar to Beck’s cognitive model of depression). Genetic
predispositions may be involved, with evidence found for mutations in the
hSERT gene linked to OCD. It may also be environmental factors, and early
life experiences (often linked to responsibility) may increase vulnerability.
Brain structure and function has also been implicated.
o OCD and the brain: Looks at anatomical and neurophysiological differences
between patients and healthy people. Some suggestion that there is
dysfunction in serotonin neurotransmission in brains with OCD, but this is not
clear enough to be diagnostic. Studies into neuropsychology have been found
between controls and patients, particularly in executive function and memory
and organisation skill. The differences are not strong enough to be used for
diagnosis.

o Cognitive behavioural model (Salkovskis, 1985): Along the same lines as

Beck, where appraisal of thoughts is central. This begins with the premise that
intrusive thoughts are normal. However, certain individuals place meaning on
these thoughts, and thus respond to them in some way (avoid, suppress,
ritualise, etc.). These responses increase vigilance for the intrusive thoughts
and protects the meaning of the intrusion. You can have OCD without having
specific overt behavioural compulsions. The response can be internal. A
diagram is below (example based on lecturer’s client): Client understood there
were no logical links to this compulsion, he allowed his mother to touch the
 letter, so the cognitive process is bizarre, and it was about working through

this.
o Cognitive factors – Intrusive thoughts might become obsessions if they are
evaluated (appraised) as: overly important (‘if I’m thinking this way, it must
be important’); highly threatening (‘if I continue to think like this, something
bad will happen’); requiring complete control (‘I’ve got to stop thinking this
way’); necessitating a high degree of certainty (‘I need to be certain that
nothing bad will happen’); associated with a state of perfection (‘I can’t stop
thinking about this until I do it perfectly’) (Clark & O’Connor, 2005).
o OCD and COVID-19: A sizable proportion of people with OCD (but not all)
experienced/reported symptom worsening during the pandemic, especially
during initial restrictions (approximately 20–65 % of cases in longitudinal
studies). There was some evidence for a particularly worse course for those
with contamination symptoms. COVID-19 became a central theme for many
people with OCD, particularly those with contamination symptoms.
Participants in specialty care reported less impact from the pandemic, which is
a ringing endorsement of psychological treatment (Guzick et al., 2021; Grant
et al., 2022; Zaccari et al., 2021).
 Body Dysmorphic Disorder
o Diagnostic criteria (distilled):
 A. Preoccupation with one or more perceived defects or flaws in
physical appearance that are not observable or appear slight to others.
(Can be to do with any part or element of the body).
 B. At some point during the course of the disorder, the individual has
performed repetitive behaviours (e.g., mirror checking, excessive
grooming, skin picking, reassurance seeking) or mental acts (e.g.,
comparing his or her appearance with that of others) in response to the
appearance concerns. (Intrusions can occur for hours a day).
 C. The preoccupation causes clinically significant distress or
impairment in social, occupational, or other important areas of
functioning.
 Specify if: With muscle dysmorphia: The individual is preoccupied
with the idea that his (more common in men) or her body build is too
 small or insufficiently muscular. This specifier is used even if the
individual is preoccupied with other body areas, which is often the
case.
o Prevalence: 0.7-2.4% in the general population (Buchanan et al., 2011). There
are higher rates among dermatology, cosmetic surgery, adult orthodontic and
oral/maxillofacial surgery patients. It is generally recognised that BDD is
highly under-diagnosed in the general population.
o Onset and course: The mean age at disorder is 16-17 years, although it is not
usually diagnosed until 10-15 years later. Patients generally present to services
for secondary or associated disorder (OCD, depression, etc.). Approximately
25% of patients attempt suicide (very concerning). The disorder is usually
chronic, although improvement is likely when evidence-based treatment is
received. Individuals with disorder onset before age 18 years are more likely
to attempt suicide, have more comorbidity, and have gradual (rather than
acute) disorder onset than those with adult-onset body dysmorphic disorder.
o Gender differences: There is no difference in prevalence rates. There are more
similarities than differences in most clinical features – for example, disliked
body areas, types of repetitive behaviours, symptom severity, suicidality,
comorbidity, illness course, and receipt of cosmetic procedures. However,
males are more likely to have genital preoccupations, and females are more
likely to have a comorbid eating disorder. Muscle dysmorphia occurs almost
exclusively in males.
o Impact on functioning: Can range from moderate (e.g. avoidance of some
social situations) to extreme and incapacitating (e.g. being completely
housebound). It impacts job, academic, or role functioning (e.g. as a parent or
caregiver), which is often severe (e.g. performing poorly, missing school or
work, not working). Social functioning is impacted (e.g. social activities,
relationships, intimacy). Psychiatric hospitalisation is often needed.
o Cognitive processes – Compared to healthy controls, individuals with BDD
(Kollei & Martin, 2014)
 Evaluate appearance more negatively;
 Endorse assumptions about appearance such as “If my appearance is
defective then I am worthless”;
 Overvalue physical appearance and attractiveness;
 Experience more anxiety and discomfort after mirror gazing;
 Experience more distress and self-focused attention after mirror
gazing;
 Engage in ruminative thinking- such as ‘Why am I so ugly’; Engage in
repeated reviews of past-appearance related experiences
o Medical interventions: Of 268 patients seeing a dermatologist, ~12% met
criteria for BDD (Phillips et al., 2000). Approx 45% of BDD patients are
seeking dermatological treatment and 23% are seeking plastic surgery
(Phillips et al., 2001). Therefore individuals with BDD make up a significant
proportion of people seeking assistance from dematology or plastic surgery,
but are unlikely to be happy with the result, may return time and again for
treatment and can be litigious.
o BDD and culture: What is deemed beautiful is determined by culture. It is
important to understand this role and how it influences their thinking and
behaviour. What is the role of culture or social pressures in the development of
BDD? Muscle dysmorphia is a key area to look at, in which certain groups in
 society have increased pressure around muscle tone and other things. There is
discussion about the role of the media here (particularly social media).
 Hoarding disorder: We get into areas that are less and less researched as we go
through the DSM in this way. OCD is well-researched, and has good treatment
outcome, but our knowledge decreases the further we get into this section. Was not
described as a stand-alone disorder till the DSM-5, it was lumped in with OCD as a
variant.
o Diagnostic criteria (distilled):
 A. Persistent difficulty discarding or parting with possessions,
regardless of their actual value.
 B. This difficulty is due to a perceived need to save the items and to
distress associated with discarding them.
 C. The difficulty discarding possessions results in the accumulation of
possessions that congest and clutter active living areas and
substantially compromises their intended use. If living areas are
uncluttered, it is only because of the interventions of third parties (e.g.,
family members, cleaners, authorities).
 D. The hoarding causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning (including
maintaining a safe environment for self and others).
 We can distinguish between people with good and poor (with a
delusional flavour) insight. A subtype of hoarding disorder is animal
hoarding, which is the accumulation of a large number of animals (e.g.
cats).
o Prevalence: There is actually no prevalence data for this in Australia. There is
some evidence to suggest they are similar to rates of BDD. There is an
estimated prevalence between 2-6% of adults in Europe and the US.
Nordsletten et al. (2013) found than 1.5% of adults in South London were
affected. This affects males and females relatively equally, but it is possibly
more common in males (although more females present for treatment). It is
more common in older adults than younger adults. This can have safety and
sanitary implications for those suffering from this disorder, so it is not an
inconsiderable issue.
o Cognitive factors: Three factors determine the difference between people who
hoard and people who don’t, involving appraisals about: control over
possessions (need to be in control of environment); concern about memory
(need to store information in case it is called for); responsibility over
possessions (possessions gain personal attributes) (after age, mood [depression
and anxiety], OCD symptoms and other OCD-related cognitive variables are
controlled for) (Steketee et al., 2003).
o Hoarding animals: The compulsive need to collect and own animals for the
sake of caring for them that results in accidental or unintentional neglect or
abuse. Animals may provide a conflict-free relationship with the individual,
unconditional love. Alternatively, perceptions of being a refuge for unloved
animals may provide the individual with a sense of purpose, a special role,
means that they are loving and caring. However, in many cases, everyone
suffers with animal hoarding—the animals, the hoarder, and those who love
the hoarder; the individual is overwhelmed by the demands of the animals
which exceeds their capacity to care for them. The RSPCA is often called in to
 deal with emaciated horses or the like, so it is an area of concern for them. It
comes about often through the best of intentions. This is quite rare.
 Trichotillomania and excoriation: Bundled together because we don’t know much
about them, and also there are lots of similarities between them which suggests
common underlying processes with different expressions.
o Trichotillomania criteria: This is highly distressing, and the changes to
physical appearance may result in avoidance and reduced wellbeing. It is
described as an itch that gets worse if you don’t scratch it, often leading to
spiralling anxiety.
 A. Recurrent pulling out of one’s hair, resulting in hair loss. (Can go
on for months or years).
 B. Repeated attempts to decrease or stop hair pulling.
 C. The hair pulling causes clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
 D. The hair pulling or hair loss is not attributable to another medical
condition (e.g., a dermatological condition).
 E. The hair pulling is not better explained by the symptoms of another
mental disorder (e.g., attempts to improve a perceived defect or flaw in
appearance in body dysmorphic disorder).
o Trichotillomania epidemiology:
 Prevalence: 1-2% adults (Stein et al., 2010). It is thought more females
are affected but more research is needed.
 Course of illness: Usually chronic but can wax and wane
 Functional consequences: Social/occupational impairment;
musculoskeletal injury (e.g., carpal tunnel syndrome; back, shoulder
and neck pain); blepharitis (inflammation of eyelids); dental damage
(e.g., worn or broken teeth due to hair biting); swallowing of hair
(trichophagia) may lead to trichobezoars (hairballs), with subsequent
anemia, abdominal pain, hematemesis, nausea and vomiting, bowel
obstruction, and even perforation (taken from DSM5). Physical
consequences can be severe.
o Excoriation (skin-picking) disorder criteria: Associated with changes in
behaviour and anxiety.
 A. Recurrent skin picking resulting in skin lesions.
 B. Repeated attempts to decrease or stop skin picking.
 C. The skin picking causes clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
 D. The skin picking is not attributable to the physiological effects of a
substance (e.g., cocaine) or another medical condition (e.g., scabies).
 E. The skin picking is not better explained by symptoms of another
mental disorder (e.g., delusions or tactile hallucinations in a psychotic
disorder, attempts to improve a perceived defect or flaw in appearance
in body dysmorphic disorder, stereotypies in stereotypic movement
disorder, or intention to harm oneself in nonsuicidal self-injury).
o Excoriation epidemiology:
 Prevalence: 1-2% of adults (Stein et al., 2010), again it is thought more
females are affected.
 Course of illness: usually chronic but can wax and wane.
 Functional consequences: social and occupational impairment; tissue
damage, scarring, infection; frequently requires antibiotic treatment for
 infection, and on occasion, it may require surgery (taken from DSM-
5).
 One challenge is differentiating between skin-picking and a self-harm
behaviour. They may both result from distress, but the intent is
different. Excoriation is likely to be less conscious.
o Psychological aspects of these disorders: People can engage in both
behaviours in a range of contexts. It is, in some people motivated by attempted
stimulation of positive mood or feelings (i.e., pleasure, gratification or relief),
or the regulation of states of high or low arousal (i.e., anxiety or boredom).
Approximately 1/5- 1/3 people with SPD or trichotillomania report being in a
trance/feeling mesmerized/experiencing depersonalisation while picking/ hair
pulling. A substantial proportion of sufferers in both groups report little or no
reflective awareness of the act as it occurs. Two subtypes of these disorders
have been proposed: “automatic pulling/picking” that occurs out of reflective
awareness in sedentary situations; “focused pulling/picking”, happens in full
awareness in response to urges or negative affective states (Snorrason et al.,
2012). There is not a lot of data exploring the psychological underpinnings of
these behaviours, and not many treatment studies.
o Psychological consequences of these disorders: They are associated with high
levels of shame, distress, and embarrassment. However, people say hair
pulling and scratching also reduces unpleasant emotions. In treating this, it is
important to really know the individual and the motivation and role of this
behaviour.
 Summary:
o OC and related disorders are considered together in the DSM because they are
all characterised to some extent by intrusive thoughts and repetitive
behaviours.
o They can all be highly distressing and associated with severe levels of
disability, dysfunction and comorbidity.
o They are all amenable to psychological treatment, but motivation is the key.
o We can recognise a theme at this point, which is that the thinking of cognitive-
behavioural psychologists and the treatment approach is around understanding
the appraisal process and looking at the avoidance behaviours that result in
this repeated pattern.

Lecture 9: Trauma and Related Disorders

 Working with trauma is part and parcel with being a clinician. There is a strong
correlational association between experiences of trauma and mental health difficulties
in general. Sometimes trauma comes about as a result of the mental health system. We
need to be aware of how our own position as clinicians impacts on our capacity to
engage with patients and work in an “objective” (never completely objective working
with individuals) manner.
 DSM-5 Trauma and Stressor Related Disorders: This is the only section in the DSM-5
that has reference to an event causally related to the disorder being described. This
seems interesting given trauma has been shown to be associated with mental health
difficulties across the board. Most people who experience trauma do not develop
mental ill-health.
 o Reactive Attachment Disorder: A solely childhood disorder involving
inappropriate attachment behaviours (not examined)
o Disinhibited Social Engagement Disorder: The essential feature involves
inappropriate overly familiar behaviour with relative strangers, also diagnosed
in childhood (not examined).
o Post-Traumatic Stress Disorder
o Acute Stress Disorder
o Adjustment Disorders
o Other Specified Trauma and Stressor Related Disorder
o Unspecified Trauma and Stressor Related Disorder
 Post-Traumatic Stress Disorder Background
o We’ll start with a few lines from “Dulce et Decorum Est” (1920) by Wilfred
Owen: “In all my dreams, before my helpless sight,/He plunges at me,
guttering, choking, drowning.” He experienced truly horrific experiences
during his time in the war, and was admitted to hospital for what was then
described as “shell shock”. These lines vividly call to mind the nightmares
Owen experienced in response to his trauma. He was returned to combat and
killed in action a week before the armistice at age 25. A novel Regeneration
by Pat Barker is a good depiction of these events, and he. Really nails PTSD
experiences.
o PTSD has been known by numerous names over time. Narratives describing
stress reactions to war and non-war events have existed for a long time.
Dickens wrote of his experiences of witnessing a railway fatality, with
numerous other examples. The Russian army in 1905 was the first group to
recognise this condition, not as PTSD. Some names include: exhausted heart;
nostalgia; battle fatigue; soldier’s heart; shell shock; combat exhaustion;
combat neurosis; battle shock; war neurosis; war strain; compensation
neurosis. These concepts have battled a lot of stigma over time. The Vietnam
War diminished a lot of this stigma, on the back of lots of lobbying from
Veterans and insurance companies in the US. This led to the development of
PTSD as a diagnosable condition by groups like the APA.
 DSM-5 Post-Traumatic Stress Disorder
o Criterion A: Exposure to actual or threatened death, serious injury, or sexual
violence in one (or more) of the following ways (this is a very explicit
definition of trauma):
 Directly experiencing the traumatic event(s).
 Witnessing, in person, the event(s) as it occurred to others.
 Learning that the traumatic event(s) occurred to a close family member
or close friend. In cases of actual or threatened death of a family
member or friend, the event(s) must have been violent or accidental.
 Experiencing repeated or extreme exposure to aversive details of the
traumatic event(s) (e.g., first responders collecting human remains;
police officers repeatedly exposed to details of child abuse).
Note: Criterion A4 does not apply to exposure through electronic
media, television, movies, or pictures, unless this exposure is work
related. (This was a very explicit change in DSM-5, partly in response
to 9/11).
 What are the kinds of events we’re talking about? The scope is very
broad. They can be war related, threatened or actual violence, disasters,
 accidents, etc. It is not enough to simply be exposed to this event,
however, for diagnosis.
o Criterion B: Presence of one (or more) of the following intrusion symptoms:
 Recurrent, involuntary, and intrusive distressing memories of the
traumatic event(s).
 Recurrent distressing dreams in which the content and/or affect of the
dream are related to the traumatic event(s).
 Dissociative reactions (e.g., flashbacks) in which the individual feels or
acts as if the traumatic event(s) were recurring.
 Intense or prolonged psychological distress at exposure to internal or
external cues that symbolize or resemble an aspect of the traumatic
event(s).
 Marked physiological reactions to internal or external cues that
symbolize or resemble an aspect of the traumatic event(s).
o Criterion C: Persistent avoidance of stimuli associated with the traumatic
event(s), beginning after the traumatic event(s) occurred, as evidenced by one
or both of the following:
 Avoidance of or efforts to avoid distressing memories, thoughts, or
feelings about or closely associated with the traumatic event(s).
 Avoidance of or efforts to avoid external reminders (people, places,
conversations, activities, objects, situations) that arouse distressing
memories, thoughts, or feelings about or closely associated with the
traumatic event(s).
o Criterion D: Negative alterations in cognitions and mood associated with the
traumatic event(s), beginning or worsening after the traumatic event(s)
occurred, as evidenced by two (or more) of the following:
 Inability to remember an important aspect of the traumatic event(s)
(typically due to dissociative amnesia and not to other factors such as
head injury, alcohol, or drugs).
 Persistent and exaggerated negative beliefs or expectations about
oneself, others, or the world (e.g., “I am bad,” “No one can be trusted,”
“The world is completely dangerous,” “My whole nervous system is
permanently ruined”).
 Persistent, distorted cognitions about the cause or consequences of the
traumatic event(s) that lead the individual to blame himself/herself or
others.
 Persistent negative emotional state (e.g., fear, horror, anger, guilt, or
shame).
 Markedly diminished interest or participation in significant activities.
 Feelings of detachment or estrangement from others.
 Persistent inability to experience positive emotions (e.g., inability to
experience happiness, satisfaction, or loving feelings).
o Criterion E: Marked alteration in arousal and reactivity associated with the
traumatic event(s), beginning or worsening after the traumatic event(s)
occurred, as evidenced by two (or more) of the following:
 Irritable behavior and angry outbursts (with little or no provocation)
typically expressed as verbal or physical aggression toward people or
objects.
 Reckless or self-destructive behavior.
 Hypervigilance.
  Exaggerated startle response.
 Problems with concentration.
 Sleep disturbance (e.g., difficulty falling or staying asleep or restless
sleep).
o F. Duration of the disturbance (Criteria B, C, D, and E) is more than 1 month.
o G. The disturbance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
o H. The disturbance is not attributable to the physiological effects of a
substance (e.g., medication, alcohol) or another medical condition.
o Specify whether – with dissociative symptoms. Specify if – With delayed
expression: If the full diagnostic criteria are not met until at least 6 months
after the event (although the onset and expression of some symptoms may be
immediate).
o Summary: TRAUMA.
 Traumatic event
 Re-experience: one of 5 symptoms
 Avoidance: one of 2 symptoms
 Unable to function: including 2 of 7 symptoms of negative alterations
in cognition/mood
 Month (at least)
 Arousal: two of 6 symptoms
 Subtypes: dissociative subtype- individual reports experiences of
depersonalization or derealization; delayed expression subtype- full
diagnostic criteria are not met until at least 6 months after the trauma.
o Bracket creep: These criteria are expansive, and some people see this as a
problem. The criteria have changed a lot over the iterations of DSM. Below is
a table showing different diagnoses in the DSM system. The MDD criteria
have not changed, and there are 227 different ways an individual could present
to meet diagnostic criteria for MDD. Specific phobias only have one way of
meeting criteria. For Panic Disorder and PTSD, we can see how many more
people could fill criteria for PTSD. What do these criteria mean in light of
this? With this huge number of presentations, do we really gain a consolidated
diagnosis at the end? This is not the case in physical illnesses. Some people
believe the criteria have expanded to be too broad.

o Moral injury: A concept gaining traction with regard to people in the military,
and a flurry of activity over COVD in relation to healthcare first responders.
People have been calling for the criterion for PTSD to emphasise moral injury
 more. This concept of moral injury broadens the understanding of trauma to
include ethical and sociological perspectives. A significant proportion of
soldiers worldwide develop feelings of shame, guilt and/or betrayal and anger
as a result of their deployment experience, with estimates ranging from
approximately 5 to 25%. “Moral injury” refers to the profound and persistent
psychological distress that people may develop when their moral expectations
and beliefs are violated by their own or other people’s actions. There is
significant overlap between PTSD and moral injury (Molendijk et al., 2022).
 Acute Stress Disorder (ASD): Symptoms emerging shortly after the onset of traumatic
events are accounted for by this disorder. IT refersto an immediate response to trauma
(criterion C.).
o DSM-5 Acute Stress Disorder Criteria: Has slightly reduced symptom
requirements. It refers to an
 A. Exposure to traumatic event- identical to Criterion A for PTSD
 B. Presence of nine (or more) of the symptoms from any of the five
categories of intrusion, negative mood, dissociation, avoidance, and
arousal, beginning or worsening after the traumatic event(s) occurred:
 C. Duration of the disturbance (symptoms in Criterion B) is 3 days to 1
month after trauma exposure.
 D. The disturbance causes clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
 E. The disturbance is not attributable to the physiological effects of a
substance (e.g., medication or alcohol) or another medical condition
(e.g., mild traumatic brain injury) and is not better explained by brief
psychotic disorder.
o Incidence: A recent meta-analysis of road accident survivors (Dai et al., 2018)
looked at 13 studies comprising 2989 patients, and found that 15.8% of
patients met criteria for ASD (using DSM-IV criteria). There is quite a lack of
epidemiological data around ASD (due to short-term nature of disorder). Is
ASD a necessary stepping stone to the development of PTSD?
 Trajectories following trauma:
o The graph below is from a study by Bryant et al. (2015), following up people
who had experienced trauma (road accidents) and were admitted to hospital
for 6 years to track their trajectory of experience in terms of stress responses
and reactions. He found 4 different patterns or trajectories: resilient, recovery,
 worsening/recovery, and chronic. What differentiates these experiences?

o This finding was essentially replicated in another study by Galatzer-Levy et al.

(2018):
 A resilient class which consistently shows few PTSD symptoms:
65.7%
 A recovery class with initial distress then gradual remission: 20.8%
 A delayed reaction class with initial low symptom levels but increased
symptoms over time: 10.6%
 A chronic distress class with consistently high PTSD levels: 8.9%
o If we can figure out what differentiates these groups, we may be able to
prevent chronic course.
 Rates of traumatic experiences: 75% of adult population (76% men and 74% of
women) experience one or more traumatic events (fitting Criterion A) in their lifetime
(Mills et al., 2011). The prevalence of trauma higher in mental health clinical
populations- up to 80% individuals. This is really high.
 Types of traumatic experiences:
o The most common events overall involve witnessing someone being badly
injured or killed, being involved in a fire or natural disaster and being involved
in life-threatening accident (all more likely to have been experienced by men).
o Men are more likely to have experienced physical attack, combat being
threatened with a weapon, held captive or kidnapped.
o Women: more likely to have experienced rape, sexual molestation, childhood
parental neglect and childhood physical abuse.
 Post-Traumatic Stress Disorder information
o Epidemiology: Despite the prevalence of trauma, the rates of developing
PTSD are quite low (referring to diagnosable levels of PTSD). The probability
of developing PTSD after a traumatic event is 8-13% in men and 20-30% in
women. The PTSD 12-month prevalence is 4.4% (McEvoy et al., 2011).
 Overall, PTSD is experienced by a minority of the population, despite the fact
the majority experience traumatic events.
o The type of trauma experienced also influences likelihood of developing

PTSD:
o The pandemic and PTSD: Higher levels of psychiatric symptomatology
including depression, anxiety, PTSD and higher levels of substance use than
expected by young people since COVID-19 has been observed. (Canada:
Craig et al., 2022)
o There was a high mental health impact experienced by healthcare workers
(Hill et al., 2022), and moral injury was also experienced by healthcare
workers (D’Alessandro et al., 2022).
o Risk factors: Our capacity to intervene with the first three of these is very

limited.
 Pre-trauma factors include (all associations, nothing causal): Gender-
female; Personality- high neuroticism; Age- young; Lower
intelligence/lower education; Neuroticism; Unstable family during
childhood; Pre-existing mood/anxiety disorder; Family history of
mood/anxiety disorder; Biological- attenuated (lower) cortisol levels.
  Trauma-related factors: Type of trauma e.g. interpersonal; Perceived
degree of life threat; Predictability and controllability; Duration and
frequency. There is limited capacity to intervene.
 Peri-traumatic reactions (at time of trauma): Arousal- heightened heart
rate in acute post trauma phase; Dissociation at time of trauma. Also
limited capacity to intervene.
 Post trauma factors (all factors reduce risk): Level of social support
and positive support; Validation of the experience; Opportunities to
‘process’ the experience. This is where we can target intervention.
o Associated features: substance use/abuse; emotional lability; impulsive and/or
self-harming behaviour; physical complaints (e.g. headaches, vague
perceptions of pain). The range of responses to trauma is huge. Is putting a
narrow framework around this actually helpful?
o PTSD and memory: A clear psychological process identified in the
development of PTSD. Should read the paper on this. It seems that the core of
PTSD has something to do with memory. These are the findings of research:
 Disturbance to the memory of the trauma itself: some people may have
remarkable clarity, others report complete amnesia for significant
aspects of a traumatic event and uncertainty and inaccuracy regarding
the sequence of events.
 Re-living experiences or ‘flashbacks’: may be triggered by recent
events/experiences different to normal autobiographical memory
because they are dominated by sensory detail but typically disjointed
and fragmented.
 Generally, individuals with PTSD have more difficulty learning,
retaining, and recalling new information. This cannot be a diagnostic
criteria, standard deviations are broad.
o The following are other psychological processes that may be involved in
prolonging a person’s reactions to a traumatic event, but are also relevant for
thinking about in clinical terms in terms of targeting treatment.
 Dissociation: “a temporary breakdown in .. the relatively continuous,
interrelated processes of perceiving the world around us, remembering
the past, or having a single identity that links out past with our future”
(Brewin & Holmes, 2003). People talk about feeling like they’re
behind a pain of glass, in a bubble, their life isn’t their own, they are
not fully involved. Sensory confusion is commonly reported, as an “out
of body” experience. Mild dissociative reactions are common under
stress- i.e. 96% soldiers undergoing survival training. They generally
can be quite common. This may impact on capacity to form memory of
the traumatic event and to integrate that memory with other memories.
They may be more at risk of longer-term PTSD. We unfortunately
don’t have good interventions for supporting people with dissociation.
It can occur with many other health difficulties. Dissociation is thought
to be a coping mechanism in some ways, enabling people to manage
distressing experiences.
 PTSD and cognitive appraisal and emotion: Appraisal of the cause of,
responsibility for, and concerns about future implications of trauma
can result in negative emotions. These appraisals are central to
treatment, as they are associated with a range of emotional reaction a
 person may describe. As clinicians, we are interested in the way they
view the trauma and its impact on their life.
 PTSD and beliefs about the world around us: We find a general
increase in negative beliefs about self, world and other found in trauma
victims suffering PTSD cf. victims not suffering PTSD. These
responses limit the person’s recovery and capacity to function.
o Aetiology of PTSD: Accounts of how PTSD develops often focus on
conditioning.
 Classical conditioning is considered, as the cues or stimuli present at
the time of the trauma are recognised by the individual, through a rapid
conditioning process, associates these stimuli with the trauma
(reactions to noise are an obvious example).

 This type of conditioning event is thought to potentially underlie the

development of PTSD through learning processes. This can be referred
to as fear conditioning. Reactions and responses then become repeated
over time with exposure to the UCS (the event itself).

 This is incorporated in a cognitive behavioural model of PTSD (Ehlers

& Clark, 2000): This really forms the underpinning of effective
treatment responses these days. Targeting the negative appraisals of the
event itself, looking at avoidance behaviours with exposure are all
avenues for treatment suggested by this model. Looking at the
 processing of memory is key. This is really difficult work, getting the
client to think about the horrible things that happened to them.

o Barriers to treatment: concerns related to stigma, shame and rejection; low

mental health literacy; lack of knowledge and treatment-related doubts; fear of
negative social consequences; limited resources, time, and expenses; specific
trauma-related barriers to mental health service use, especially concerns about
re-experiencing the traumatic events (Kantor et al., 2017). Given that
treatment is shown to be beneficial and often necessary for recovery, these are
significant issues. The Victorian Royal Commission recommended stopping
restraint practices and restrictions on isolation.
 Complex PTSD: Associated with chronic and repeated traumatic events. Some people
in the PTSD field believe that this repeated and chronic experience can result in a
different presentation to regular PTSD, and this has been termed “complex PTSD”.
o This includes the symptoms of PTSD, but also the development of persistent
and pervasive impairments in affective, self and relational functioning
including: Emotion Dysregulation (“I react intensely to all sorts of things”);
Interpersonal dysfunction (“My relationships have extreme ups and downs”);
Difficulties in self-identity (“I feel empty or hollow inside”).
o This add-on to “regular” PTSD can mean that individuals don’t respond as
well to treatments we have developed for normal PTSD, and there needs to be
something else in the treatment to address this additional category. There was
a lot of discussion about including this category in the DSM-5 but failed.
Interestingly, this did make it into the ICD-10. The lecturer supports the
evidence for this separate group of people that warrant a slightly different
approach in treatment.
o Differentiating PTSD from complex PTSD: Cloitre et al. (2013) conducted a
Latent Profile Analysis on assessment data from 302 treatment-seeking
individuals with diverse trauma histories, ranging from single events (e.g.,
9/11 attacks) to sustained exposures (e.g., childhood or adult physical and/or
sexual abuse). This is the most comprehensive of these studies, but many other
studies have been designed in the same vein, trying to tease out the difference
between these experiences. Results: Three distinct groups were found – one
 didn’t report PTSD symptoms, one reported high levels of PTSD symptoms
but low levels of complex symptoms, and the last group (about a third)
reported high levels of all symptoms. This appeared to be robust evidence, but
people questioned whether this was due to overlap with BPD. The second
figure shows results from this study, which still shows a distinct CPTSD
cohort. This won over the ICD but not the DSM, but they will probably
change their mind.

 Adjustment disorder:
o DSM-5 criteria: Note that these descriptions are really characterised by
vagueness, as opposed to the PTSD diagnosis that is almost over-described.
 A. The development of emotional or behavioral symptoms in response
to an identifiable stressor(s) occurring within 3 months of the onset of
the stressor(s). (All in the eye of the beholder)
  B. These symptoms or behaviors are clinically significant, as
evidenced by one or both of the following: Marked distress that is out
of proportion to the severity or intensity of the stressor, taking into
account the external context and the cultural factors that might
influence symptom severity and presentation; Significant impairment
in social, occupational, or other important areas of functioning. (These
symptom responses are vague).
 C. The stress-related disturbance does not meet the criteria for another
mental disorder and is not merely an exacerbation of a preexisting
mental disorder.
 D. The symptoms do not represent normal bereavement.
 E. Once the stressor or its consequences have terminated, the
symptoms do not persist for more than an additional 6 months.
(Supposed to be short-term reaction.)
o There are lots of subtypes in the DSM-5:
 With depressed mood: Low mood, tearfulness, or feelings of
hopelessness are predominant.
 With anxiety: Nervousness, worry, jitteriness, or separation anxiety is
predominant.
 With mixed anxiety and depressed mood: A combination of depression
and anxiety is predominant.
 With disturbance of conduct: Disturbance of conduct is predominant.
 With mixed disturbance of emotions and conduct: Both emotional
symptoms (e.g., depression, anxiety) and a disturbance of conduct are
predominant.
 Unspecified: For maladaptive reactions that are not classifiable as one
of the specific subtypes of adjustment disorder.
o This diagnosis is critiqued for its vagueness. It is viewed as a bit of a rag-bag
diagnosis.
o ICD-11 Adjustment Disorder: These criteria are more specific
 Essential (Required) Features: A maladaptive reaction to an
identifiable psychosocial stressor or multiple stressors (e.g., single
stressful event, ongoing psychosocial difficulty or a combination of
stressful life situations) that usually emerges within a month of the
stressor. Examples include divorce or loss of a relationship, loss of a
job, diagnosis of an illness, recent onset of a disability, and conflicts at
home or work./The reaction to the stressor is characterized by
preoccupation with the stressor or its consequences, including
excessive worry, recurrent and distressing thoughts about the stressor,
or constant rumination about its implications. (different from
DSM)/Once the stressor and its consequences have ended, the
symptoms resolve within 6 months.
 Additional Clinical Features: Symptoms of preoccupation may worsen
with reminders of the stressor(s), resulting in avoidance of stimuli,
thoughts, feelings or discussions associated with the stressor(s) to
prevent preoccupation or distress. (different from DSM)/Additional
psychological symptoms of Adjustment Disorder may include
depressive or anxiety symptoms as well as impulsive ‘externalizing’
symptoms, particularly increased tobacco, alcohol, or other substance
use./Symptoms of Adjustment Disorders usually abate when the
 stressor is removed, when sufficient support is provided, or when the
affected person develops additional coping mechanisms or strategy.
 Defining features of preoccupation: Preoccupation contains factual
(neutral) thoughts. Thoughts in preoccupation are stressor-related.
Preoccupation is time-consuming. Preoccupation is often associated
with negative emotions (Eberle and Maercker, 2021).
o Epidemiology: We don’t know much but it is quite a commonly used
diagnosis. This information below doesn’t mean much.
 Almost three times as common as major depression (13.7 vs. 5.1%) in
acutely ill medical in-patients (Silverstone et al., 1996)
 Diagnosed in up to one third of cancer patients experiencing a
recurrence (Okamura et al., 2002)
 Primary care- rates varying from 1-18% people seen for mental health
problems (Casey et al., 1984; Blacker et al., 1988)
 Among psychiatric inpatients, 9% of consecutive admissions to an
acute public sector unit were diagnosed with adjustment disorder
(Koran et al., 2003)
o Problems with this disorder:
 There is no standardised diagnostic assessment tool
 It has not been included in any of the major epidemiological studies
(such as the Epidemiological Catchment Area Study, the National
Comorbidity Survey, Aust National Mental Health survey).
 Does this medicalise ‘problems of living’? This is particularly
concerning.
 Is it just a “wastebasket diagnosis” for those who fail to meet the
criteria for other disorders?
 We do not even know levels of comorbidity.
 Best practice treatment? We have no idea about treatment. Clinical
utility is questionable. (see O’Donnell et al., 2018)
 Read review by Bachem and Casey 2018
 Trauma and Stressor Related Disorders Summary:
o Considered together in DSM because they all preceded by the experience of a
traumatic or stressful event. But many people who experience trauma do not
develop one of these disorders.
o For a long time, PTSD sufferers were discriminated against. Activism during
and after the Vietnam war finally saw PTSD ‘officially’ recognised as a
mental disorder;
o Complex PTSD: associated with chronic and repeated trauma and includes
symptoms of PTSD AND persistent and pervasive impairments in affective,
self and relational functioning
o Adjustment Disorder: one of the most frequently diagnosed mental disorders
but defined as a low-threshold or a diagnosis of exclusion.
 Siegfried Sassoon: Was in the hospital with Wilfred Owen, threw his Victoria Cross
in the Thames and championed his friend’s poetry. He offers a clear depiction of
people who develop PTSD: "How many a brief bombardment had its long-delayed
after-effect in the minds of these survivors, many of whom had looked at their
companions and laughed while the inferno did its best to destroy them. Not then was
their evil hour, but now; now, in the sweating, suffocation of nightmare, in paralysis
of limbs, in the stammering of dislocated speech. Worst of all, in the disintegration of
those qualities through which they had been so gallant and selfless and uncomplaining
 - this, in the finer types of men, was the unspeakable tragedy of shell shock". From
Sherston's Progress (1936).

Prac 4

 Really good discussion about “Hearing Voices”. Very anti-psyc .

Lecture 10: Addictive Disorders

 What is included in this section of the DSM-5? It is divided into two bits, not equal in
size:
o 'Substance-related disorders’: references 10 separate classes of drugs that can
directly activate the brain reward systems, and can produce such an intense
activation of the reward system that normal activities may be neglected. These
are: alcohol; caffeine; cannabis; hallucinogens; inhalants; opioids; sedatives;
hypnotics;  anxiolytics; stimulants; tobacco; and other (or unknown)
substances.
o Gambling disorder: inclusion reflects evidence that gambling behaviors
activate reward systems similar to those activated by drugs of abuse and that
produce some behavioral symptoms that appear comparable to those produced
by the substance use disorders. This is included in the DSM-5 because of the
extensive research showing that gambling produces similar chemicals in the
brain as drugs.
 Substance Use Disorders (SUD)
o Basic definition: A substance use disorder (SUD) is a treatable mental disorder
that affects a person’s brain and behavior, leading to their inability to control
their use of substances like legal or illegal drugs, alcohol, or
medications. Symptoms can be moderate to severe, with dependence being the
most severe form of SUD. People with a SUD may also have other mental
health disorders, and people with mental health disorders may also struggle
with substance use. 
o Co-occurring substance use and other mental disorders is more often the rule
rather than the exception and is associated with poorer outcomes across the
board. This means a poorer prognosis (more likely to become chronic and
disabled), higher utilisation of services, greater stigma, and higher illness
burden.
o Co-occurrence of mental health disorders and SUD: Is there a direct causal
relationship between these two things (in either direction)? Is there an indirect
causal relationship (involving an extraneous factor)? Are there common
factors that increase the risk of both disorders? There is evidence for all these
 things, but it is something we want to understand better.

o Attitudes towards substance use over history (Nathan et al., 2016): This is
such a fun narrative, interesting demonstration of how it’s about how you tell
the story.
 Ancient writings (Egyptian, Greek, early Christian) wrote of negative
impact of too much alcohol on behaviour and thought processes.
 Middle ages: alcohol was preferred to water because of the lack of
clean water, Christian church emphasized idea of ‘moderation’, use
beyond ‘moderation’ was viewed as a character flaw for succumbing to
temptation (latter an issue of the spirit). This is a moral explanation.
 Early psychiatrists (Pinel, Rush, Kraepelin, Bleuler) began to promote
the idea that addiction was a medical illness, moving away from the
moral account.
 Current separation of drug/alcohol treatment from other mental health
treatment is partially a function of the historic separation (drug/alcohol
abuse thought to be indicative of weak character).
o Terminology of a substance:
 Use: Any use of a given substance/drug
 Misuse: Harmful use of substances (incl. use for non-medicinal
purposes)
 Abuse (DSMIV Category): A pattern of repeated drug or alcohol use
that often interferes with health, work or social relationships
 Dependence (DSM-IV Category): an adaptive state that develops from
repeated drug administration, and which results in (physical and/or
psychological) withdrawal upon cessation of drug use
 Use Disorder (DSM5 Category): takes the place of Abuse/Dependence
as of DSM5
o What is addiction? The term we often use to indicate the disease process
underlying a substance use disorder or problematic behavioural compulsion
(e.g., gambling). Note that addiction itself is not a diagnosis or a medical label.
The DSM-5 avoids this term. We try to avoid talking about “addicts” and
pejorative language in this space.
 DSM-5: Substance-Related and Addictive Disorders. The DSM-5 approach is to
divide these disorders into two groups – substance-induced disorders and substance
use disorders. We will look at SUDs first.
 DSM-5 Substance Use Disorders: The “essential feature…is a cluster of cognitive,
behavioral, and physiological symptoms indicating that the individual continues using
the substance despite significant substance-related problems.” There is an underlying
assumption here that this continued use is due to some underlying change in neural
circuitry that may persist beyond intoxication, and that the behavioural effects of
these brain changes are that the individual continues to seek the substance and
preference its use over other activities in life. General diagnostic criteria:
o Impaired control over substance use:
 The individual may take the substance in larger amounts or over a
longer period than was originally intended
 The individual may express a persistent desire to cut down or regulate
substance use and may report multiple unsuccessful efforts to decrease
or discontinue use
 The individual may spend a great deal of time obtaining the substance,
using the substance, or recovering from its effects.
 Craving: An intense desire or urge for the drug that may occur at any
time but is more likely when in an environment where the drug
previously was obtained or used.
o Social impairment:
 Recurrent substance use may result in a failure to fulfil major role
obligations at work, school, or home
 The individual may continue substance use despite having persistent or
recurrent social or interpersonal problems caused or exacerbated by the
effects of the substance
 Important social, occupational, or recreational activities may be given
up or reduced because of substance use
o Risky use of the substance
 Recurrent substance use in situations in which it is physically
hazardous
 The individual may continue substance use despite knowledge of
having a persistent or recurrent physical or psychological problem that
is likely to have been caused or exacerbated by the substance
o Pharmacological criteria
 Tolerance is signalled by requiring a markedly increased dose of the
substance to achieve the desired effect or a markedly reduced effect
when the usual dose is consumed.
 Withdrawal is a syndrome that occurs when blood or tissue
concentrations of a substance decline in an individual who had
maintained prolonged heavy use of the substance. After developing
withdrawal symptoms, the individual is likely to consume the
substance to relieve the symptoms
o Severity of disorder:
 a Mild substance use disorder is suggested by the presence of two to
three symptoms,
 Moderate by four to five symptoms, and
 Severe by six or more symptoms.
  Course specifiers and descriptive features specifiers: “in early
remission,”; “in sustained remission,”; “on maintenance therapy,”; “in
a controlled environment.”
 DSM-5 Alcohol Use Disorder (same 11 symptom description as above now specified
for alcohol):
o A problematic pattern of alcohol use leading to clinically significant
impairment or distress, as manifested by at least two of the following,
occurring within a 12-month period:
 Alcohol is often taken in larger amounts or over a longer period than
was intended.
 There is a persistent desire or unsuccessful efforts to cut down or
control alcohol use.
 A great deal of time is spent in activities necessary to obtain alcohol,
use alcohol, or recover from its effects.
 Craving, or a strong desire or urge to use alcohol.
 Recurrent alcohol use resulting in a failure to fulfill major role
obligations at work, school, or home.
 Continued alcohol use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of alcohol.
 Important social, occupational, or recreational activities are given up or
reduced because of alcohol use.
 Recurrent alcohol use in situations in which it is physically hazardous.
 Alcohol use is continued despite knowledge of having a persistent or
recurrent physical or psychological problem that is likely to have been
caused or exacerbated by alcohol.
 Tolerance, as defined by either of the following: A need for markedly
increased amounts of alcohol to achieve intoxication or desired effect;
A markedly diminished effect with continued use of the same amount
of alcohol.
 Withdrawal, as manifested by either of the following: The
characteristic withdrawal syndrome for alcohol (refer to Criteria A and
B of the criteria set for alcohol withdrawal); Alcohol (or a closely
related substance, such as a benzodiazepine) is taken to relieve or
avoid withdrawal symptoms.

o Specify if:
 In early remission: After full criteria for alcohol use disorder were
previously met, none of the criteria for alcohol use disorder have been
met for at least 3 months but for less than 12 months (with the
exception that Criterion A4, “Craving, or a strong desire or urge to use
alcohol,” may be met).
 In sustained remission: After full criteria for alcohol use disorder were
previously met, none of the criteria for alcohol use disorder have been
met at any time during a period of 12 months or longer (with the
exception that Criterion A4, “Craving, or a strong desire or urge to use
alcohol,” may be met).
 In a controlled environment: This additional specifier is used if the
individual is in an environment where access to alcohol is restricted.
o Specify current severity:
 Mild: Presence of 2–3 symptoms.
  Moderate: Presence of 4–5 symptoms.
 Severe: Presence of 6 or more symptoms.
 The DSM-5 goes through and has similar symptom specifiers for: caffeine; opioids;
tabacco; cannabis; hallucinogens; sedatives; inhalants; hypnotics; anxiolytics;
stimulants; and other (or unknown) substances.
 Substance Induced Disorders: These are divided further into three groups –
intoxication, withdrawal, other substance/medication induced mental disorders.
General diagnostic criteria (broad):

o Disorder associated with Substance Intoxication

 The essential feature is the development of a reversible substance-
specific syndrome due to the recent ingestion of a substance
 The clinically significant problematic behavioural or psychological
changes associated with intoxication (e.g., belligerence, mood lability,
impaired judgment) are attributable to the physiological effects of the
substance on the central nervous system and develop during or shortly
after use of the substance
 The symptoms are not attributable to another medical condition and are
not better explained by another mental disorder
o Disorder associated with Substance Withdrawal
 The essential feature is the development of a substance-specific
problematic behavioral change, with physiological and cognitive
concomitants, that is due to the cessation of, or reduction in, heavy and
prolonged substance use.
 The substance-specific syndrome causes clinically significant distress
or impairment in social, occupational, or other important areas of
functioning (behavioural change).
 The symptoms are not due to another medical condition and are not
better explained by another mental disorder.
 DSM-5 Alcohol intoxication (also specific criteria for each of the 10 classes):
o A. Recent ingestion of alcohol.
o B. Clinically significant problematic behavioral or psychological changes
(e.g., inappropriate sexual or aggressive behavior, mood lability, impaired
judgment) that developed during, or shortly after, alcohol ingestion.
o C. One (or more) of the following signs or symptoms developing during, or
shortly after, alcohol use:
  Slurred speech;
 Incoordination;
 Unsteady gait;
 Nystagmus;
 Impairment in attention or memory;
 Stupor or coma.
o D. The signs or symptoms are not attributable to another medical condition
and are not better explained by another mental disorder, including intoxication
with another substance.
 DSM-5 Alcohol Withdrawal (also specific criteria for each of the 10 classes):
o A. Cessation of (or reduction in) alcohol use that has been heavy and
prolonged.
o B. Two (or more) of the following, developing within several hours to a few
days after the cessation of (or reduction in) alcohol use described in Criterion
A:
 Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100
bpm).
 Increased hand tremor.
 Insomnia.
 Nausea or vomiting.
 Transient visual, tactile, or auditory hallucinations or illusions.
 Psychomotor agitation.
 Anxiety.
 Generalized tonic-clonic seizures.
o C. The signs or symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
o D. The signs or symptoms are not attributable to another medical condition
and are not better explained by another mental disorder, including intoxication
or withdrawal from another substance.
o Specify if: With perceptual disturbances: This specifier applies in the rare
instance when hallucinations (usually visual or tactile) occur with intact reality
testing, or auditory, visual, or tactile illusions occur in the absence of a
delirium.
 DSM-5 Substance/medication-induced mental disorders: All substance/medication-
induced disorders share common characteristics:
o The disorder represents a clinically significant symptomatic presentation of a
relevant mental disorder.
o There is evidence from the history, physical examination, or laboratory
findings of both of the following:
 The disorder developed during or within 1 month of a substance
intoxication or withdrawal or taking a medication; and
 The involved substance/medication is capable of producing the mental
disorder.
o The disorder is not better explained by an independent mental disorder (i.e.,
one that is not substance- or medication-induced). Such evidence of an
independent mental disorder could include the following:
 The disorder preceded the onset of severe intoxication or withdrawal or
exposure to the medication; or
  The full mental disorder persisted for a substantial period of time (e.g.,
at least 1 month) after the cessation of acute withdrawal or severe
intoxication or taking the medication. This criterion does not apply to
substance-induced neurocognitive disorders or hallucinogen persisting
perception disorder, which persist beyond the cessation of acute
intoxication or withdrawal.
o The disorder does not occur exclusively during the course of a delirium.
o The disorder causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
o Types of symptoms that can be differentiated:
 Substance intoxication delirium
 Substance withdrawal delirium
 S-I persisting dementia
 S-I persisting amnestic disorder
 S-I psychotic disorder
 S-I mood disorder
 S-I anxiety disorder
 S-I sexual dysfunction
 S-I sleep disorder
 Epidemiology of SUD (substance use in general):
o Which substances are used? Global Drug Survey (2018)

o Drug use in Australia: Substance use is common. SUD is less common. What
differentiates people who can use substances in a “healthy” way and those
 who can’t?

o Most common initial (illicit) drug: US National Institute on Drug Abuse

o Age of peak use:

o Why do people use drugs/substances? There are well-documented ritual and

cultural uses of substances (e.g. wine in the Catholic church). Many
 substances have an important role in health, with medical and therapeutic use
of substances. Both of these are sanctioned uses. Substances are used for
social and recreational purposes. There may be occupational or functional
reasons to use substances (dexamphetamine for students, or truck drivers).
o Who is more likely to develop SUD? Demographic correlates:
 Age of illicit users: highest amongst 18-25 (have higher risk of
developing disorder)
 Males significantly more likely to use
 Urban dwellers more likely than non-metro
 Regional differences exist (also influenced by industry, geography,
cultural groups)
 In USA black more likely to be illicit users, Indigenous Australians
more likely to use harmful amounts of alcohol than non-Indigenous
 Psychiatric patients use higher amounts
o Delker et al. (2015): Demonstrates alcohol abuse disorder is most prevalent.

o SUD Epidemiology: Drug dependence is the single largest contributor to

disease burden affecting Australians. Alcohol abuse and cigarette smoking are
the two highest causes of preventable deaths (app. 15,000 per year). 38% of
Australians have used an illicit drug during their lifetime. 9% have used a
psychostimulant in the last 12 months.
o Dependence among users: Anthony et al. (1994)
35
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% of Users Who are Dependent

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o Dependence (Lopez-Quintero et al., 2011): Levels of dependence are highest
amongst tobacco users, and alcohol and tobacco are next, and lowest in
marijuana.

o Abuse potential: Some substances have a higher potential for the development
of problematic use, based on the physiological actions of the substance. It
partially relates to how quickly a drug has its effects, which varies by drug and
route of administration. In general, the quicker the drug ‘acts’, the faster it
usually stops acting. Half-life (how long it takes for your body to clear a drug)
is also important to abuse potential. Quick up, quick down = high abuse
potential. E.g. heroin acts very fast, but its half-life is shorter than many other
drugs, meaning it has a higher abuse potential.
o Withdrawal: Influences the potential for problematic use developing. The
more severe the withdrawal, the higher the likelihood someone will retake it to
alleviate the effects.
 Caffeine: Withdrawal effects of caffeine can reliably be demonstrated
in nearly 100% of individuals with as little as 100mg of caffeine per
day (1 cup of coffee). Withdrawal entails: Headache; Fatigue; Anxiety;
Concentration Difficulties; Depression/Flat Affect; Irritability;
Tremors; Low Energy. It has high reuse potential because withdrawal
effects are unpleasant, and it doesn’t take much coffee to alleviate
these symptoms.
 Alcohol: These are quite severe. The potential of reuse is very high.
Symptoms: Tremor; Insomnia; Nausea/Vomiting; Transient
hallucinations; Psychomotor agitation; Anxiety; Seizures. Withdrawal
can actually be dangerous, even life-threatening, so medically
supervised withdrawal is often required. Delirium tremens can develop
(5-20% of patients undergoing detox): hyperadrenergic state,
disorientation, tremors, diaphoresis, impaired attention/consciousness,
and visual and auditory hallucinations
 Cannabis: Withdrawal is reported in about 1/3 of users in the general
population and reported by 50-95% of heavy users (Hasin et al., 2013).
 Symptoms are listed below (Budney & Hughes, 2012).

 Aetiology of problematic drug use: Why do people develop problematic drug use?
Why are some people more vulnerable than others? There are a number of models that
have been proposed.
o “Moral” models: Problematic drug use is attributed to moral weakness, or an
“addictive personality”. This is characterised by sensation/novelty seeking,
impulsivity, impaired future time orientation/consideration of future
consequences, harm avoidance and reward dependence. This is still current in
some sectors of the community. The root cause of problematic use is a lack of
willpower due to poor moral development. There is a lack of any compelling
evidence for a moral underpinning for SUDs. This type of approach assumes
that substance use in general is evil. It is very pejorative. People are viewed as
helpless, and that it is an inevitability that this would happen. We just throw
the person out the window.
o “Disease” models: The substance use is caused by some pathology in the
individual that results in this weakness, which “causes” further problems. The
use of a drug outside of a medical setting is an abnormality. The user is sick
and needs treatment. It may not be a moral failing, but they have still failed for
not managing use. Treatment is cessation of use. This is broadly an
Enlightenment kind of model, in which addiction is a disease that is lifelong
and progressive. To change, the “addict” must become enlightened, by
realising that change is possible only by relinquishing personal control to a
“higher power”.
o The “enlightenment” model is the kind of thing behind a program like
Alcoholics Anonymous. There model is as follows: ‘Alcoholism’ is a disease
characterized as a unique and progressive condition that is both qualitatively
and quantitatively different from normality (there is something wrong and
different about these people). The cardinal symptom of alcoholism is loss of
control over alcohol, the inability to restrain oneself from further drinking (e.g.
"One drink, one drunk"). The disease is understood to be irreversible,
incapable of being cured, but possible to arrested through total abstinence
from drinking alcohol. The intervention implications of this are as follows:
Individuals with this condition should be identified, informed of their
abnormal condition, brought to accept the diagnosis and then persuaded to
abstain from drinking alcohol for the rest of their lives. Relies heavily on peer
support for the treatment. Some people find this useful, and it can work. The
organization has not allowed people to conduct studies (RCTs) on whether this
 treatment is effective, rather promoting good news stories without empirical
evidence. Many people who work in the area recoil at the pejorative aspect of
this approach (the view that the individual lacks control).
o information. People use substances due to ignorance. Therefore, when armed
with correct information about the dangerous effects of alcohol or drugs,
individuals are presumed to be less likely to use alcohol in a hazardous
fashion. Treatment under this model is education of patients about the dangers
of drinking and use of drugs. A lot of government implementation is based on
this (e.g. drink driving). We know that this doesn’t stop people from
developing problematic levels of substance use. It may be preventative, but
they are not sufficient in themselves to address levels of problematic substance
use.
o Social learning: Has a huge role to play. This model suggests drug use is
learned and can be functional. It focuses on the interaction between the
individual, the social environment, and other factors. It suggests drug use can
be learned and reinforced by peers, family, partners, and the media more
generally. It does not claim it is good or bad and suggests a cost/benefit ratio
around drug use, and it needs to be understood within this ratio.
Parenting/familial influence can be permissive, leading to substance use
commencement. Environment also plays a role; an individual may never have
used if not exposed to a certain situation. The Social Economic System
influences which drugs are popular, e.g. cocaine in the 80s, MDMA in the 90s,
alcohol in depression era 1930s. Cultural factors like religion also play a role,
as well as the influences of peers. Socialisation and social skills may also
create normative behaviour that leads to substance use (e.g. beer at a bbq).
o Operant conditioning: Behaviour reoccurring is dependent on reinforcement
(rewards/punishment based). With substance use, we are usually in an
environment where we are more relaxed and engaged with the social
environment, with positive feedback for using the substance. This reward
makes people more likely to use the substance again. There is a clear
relationship here.
o Classical conditioning: Where stimuli a repeatedly paired, and the response
first elicited from the one stimulus becomes elicited by the other stimuli. This
is also very relevant for substance use (maybe work this out), particularly in
terms of addiction mechanisms (the UCS comes to prompt use). These types
of models give us entry into treatment.
o Biological (Koob & Volkow, 2016): Deficits in neural circuitry underpinning
incentive salience, executive function, and abnormal reward/stress resp. fuel
addiction cycle of binge/intoxication, withdrawal, and preoccupation. One
talked about often is the dopaminergic reward system – use of a substance
increases dopamine that give us rewards. Serotonin and endorphins also play a
role. Genetic factors may also play a role. We understand a bit of this, but it is
very complex and the difference between substances makes it difficult. No
 model is preferentialised.

o Biopsychosocial model: This is the overwhelmingly endorsed model by

governments, health organizations (WHO), and many treatment programs.
Considers the etiology of addiction to be a multifactorial phenomenon
consisting of biological, psychological and social components. It looks at the
whole individual and the interaction of multiple factors in determining
progression. This rejects a reductionistic view of addiction (such as the moral
model) and emphasizes that it is the result of several forces (society
contributes to problematic drug use); it "is a primary, chronic disease with
genetic, psychosocial and environmental factors influencing its development
and manifestation. The disease is often progressive and fatal.". In terms of
treatment, this model suggests we need to look at the individual’s place in
society, their development, and any other factors that contribute to how they
have got to this problematic position. The underlying assumption of this model
is that drug use is universal. Humans are born with the drive to experiment
early in life. We receive rewards and punishment for trying various ways of
using substances. We develop preferred methods and tend to persist in
attempts. This is shaped by psycho-social processes (desires, availability
norms, etc.). Set (people) and setting (environment) shape experience (can be
positive and valuable).
o Public health model: The biopsychosocial model gives us good avenues for
intervention that is not stigmatising and works with the individual. The
individual is provided with choice. Below is from our Department of Health
and Ageing. This gives us avenues for treatment that can focus on the
 availability of drugs, the individual, the community, and the media.

 Treatment:
o Prohibition/legalisation: We know this doesn’t work. In the graph below, the
red line shows the period of prohibition of alcohol. Increases in black market
use of substances results in the use of unregulated substances that are often
more dangerous. We see similar graphs with things like heroin, and if we look
at countries with more permissive levels of substance use, we see different
patterns. The measures are not sufficient.

o SUD treatment typically entails: psychotherapy and/or behavioural

counselling; medication (e.g. for alcohol withdrawal medication, or opioid
 agonist treatments like methodone); management of withdrawal symptoms;
evaluation/treatment for co-occurring mental health conditions; relapse
prevention; detoxification.
o Psychological approaches to treatment of SUD:
 Alcoholics/Narcotics Anonymous: Group-based treatment based on
principles of 12-steps (abstinence).
 Behavioural therapy: Contingency management, using principles of
reinforcement, reward, and punishment.
 Cognitive behavioural therapy: Recognition of triggers/cues for use
and facilitation of coping strategies.
 Harm reduction/minimisation: Goal of reducing harmful use to less
harmful use or reducing means of use to less harmful approach.
 Motivational enhancement therapy: Effort to facilitate movement
through stages of change.
o Harm reduction/minimisation: Very much the core to mainstream approach
taken to SUD at the moment. The goal may not be abstinence, but just
reduction to medium or low risk.

o Motivation stages of change: About behavioural change in general (Prochaska

& DiClemente, 1983). This is a model underpinning some of the most
 efficacious psychological approaches at the moment. Lots of evidence behind

this.
o The public health model also incorporates the stages of change approach. It
recognises that people may dip in and out of treatment with various levels of
success. This is actually just part of the process.
o Examples of harm minimisation programs: Needle and syringe programs
(yellow bins in toilets, been in place for over 30 years providing sterile
equipment for users); Medication-assisted Treatment for Opioid Dependence
(methodone and other programs, high levels of efficacy); Diversion programs
(instead of getting a criminal record, they are directed to treatment approaches,
higher effectiveness than incarceration); sobering up services.
 Gambling disorder:
o DSM-5 Criteria (modelled on SUD criteria): A diagnosis of gambling disorder
requires at least four of the following during the past year:
 Need to gamble with increasing amount of money to achieve the
desired excitement. (related to tolerance)
 Restless or irritable when trying to cut down or stop gambling.
(withdrawal)
 Repeated unsuccessful efforts to control, cut back on or stop gambling.
(loss of control)
 Frequent thoughts about gambling (such as reliving past gambling
experiences, planning the next gambling venture, thinking of ways to
get money to gamble).
 Often gambling when feeling distressed.
 After losing money gambling, often returning to get even (referred to
as “chasing” one’s losses)
 Lying to conceal gambling activity
 Jeopardising or losing a significant relationship, job or
educational/career opportunity because of gambling.
 Relying on others to help with money problems caused by gambling.
o Epidemiology: 70% of Australians have participated in some form of
gambling over the past year. Estimates suggest about 1% of population meets
criteria with 4% at risk (about same rate as schizophrenia). Across countries,
there is some variability, with a range of about 1-5%. In countries where
gambling is not heavily regulated (e.g., Australia), rates are higher than
 countries where it is regulated (e.g., USA) (Browning, 2013). The reliance on
gambling revenue by governments is abhorrent.
o Problem gambling in Australia: Problems tend to be concentrated more highly
in certain demographic groups: Males (usually 60% at the population level);
younger people (aged 18–35 years); Aboriginal people; people who are not in
a stable relationship; and among lower socioeconomic groups. Problem
gamblers also tend to have: a greater likelihood of having started gambling at
a young age; to have experienced larger wins when they first started gambling;
and to have a history of problem gambling in their families.
o Aetiology: Electronic gaming machines are most popular form of gambling.
Gambling machines typically operate on a schedule of intermittent
reinforcement (manufacturers make no bones about using psychology). This is
the strongest type of behavioral learning. There are undoubtedly
neurobiological, cognitive, and personality factors that contribute as well, but
the influence of learning is most well understood.
 DSM-5 further study required: Internet Gaming Disorder. Defined as: “…a pattern of
excessive and prolonged Internet gaming that results in a cluster of cognitive and
behavioral symptoms, including progressive loss of control over gaming, tolerance,
and withdrawal symptoms, analogous to the symptoms of substance use disorders.
(DSM5) We need a better understanding of aetiology and epidemiology before it gets
a listing in the DSM-5.
 From last lecture, EMDR is mainstream treatment approach for PTSD.

Lecture 11: Personality Disorders

 Some definitions:
o Personality: Personality refers to individual differences in characteristic
patterns of thinking, feeling and behaving.
o Personality disorder: An enduring pattern of inner experience and behaviour
that deviates markedly from the expectations of the individual’s culture and is
manifested in 2 or more of the following areas: Cognition (ways of thinking
and interpreting self, others, events); Affectivity (range, intensity, lability and
appropriateness of emotional response.); Interpersonal functioning; Impulse
control.
 Core feature of Personality Disorders (not in DSM)
o Functional inflexibility: Failure in adaptation to changing and varied life
experience; A tendency to rigidly apply a range of behavioural strategies or
responses across diverse life situations - even when inappropriate
o Self-defeating behaviour patterns: Typical ways of responding or coping that
worsen the current situation or are explicitly damaging for the person.
Nevertheless, the person demonstrates limited capacity to intervene
constructively or to learn from experience.
o Tenuous stability under stress: Marked instability in mood, thinking and
behaviour during difficult periods.
 DSM-5 Personality Disorders:
o Were first introduced in a systematic fashion by the DSM-III in 1980 (quite
late). They were considered an “Axis II” disorder until DSM-5 removes the
axis system completely. This is because personality disorders a considered to
be “trait-based” rather than “state-based” (Axis I). This was changed to
 encourage clinicians to think of PDs as co-existing with Axis I disorders (there
is high comorbidity). PDs interact with “Axis I” disorders which influences
impact presentation, treatment adherence, response, etc. Lecturer did find
differentiation helpful in considering the impact of personality on both kinds
of disorders.

o DSM-5 General Diagnostic Criteria:

 A. An enduring pattern of inner experience and behaviour that deviates
markedly from the expectations of the individual’s culture (it is very
important to consider culture in this area). The pattern is manifested in
two (or more) of the following: Cognition (i.e. ways of perceiving and
interpreting self, other people, and events); Affectivity (i.e. the range,
intensity, lability, and appropriateness of emotional response);
Interpersonal functioning; Impulse control.
 B. The enduring pattern is inflexible and pervasive across a broad
range of personal and social situations.
 C. Leads to clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
 D. The pattern is stable and of long duration, and its onset can be
traced back at least to adolescence or early adulthood.
 E. Not better explained as a manifestation or consequence of another
disorder.
 F. Not due to physiological effects of substance or medical condition.
o There are 3 clusters of personality disorders in the DSM-5:
 Cluster A: Paranoid PD; Schizoid PD; Schizotypal PD.
 Cluster B (most well-researched): Antisocial PD; Borderline PD;
Histrionic PD; Narcissistic PD.
 Cluster C: Avoidant PD; Dependent PD; Obsessive-compulsive PD
 Other: Personality change due to another medical condition; other
specified/unspecified personality disorder.
 Paranoid PD (cluster A):
o Diagnostic criteria (distilled):
 A. A pattern of distrust and suspiciousness such that others’ motives
are interpreted as malevolent. Includes: Suspicious of others, questions
loyalty of friends/associates, reluctant to confide as expect to be
exploited, reads hidden messages onto benign remarks, bears grudges,
easily slighted and quick to retaliate, suspicious of fidelity of partner.
 B. Does not occur exclusively during schizophrenia or other disorder
with psychotic features, or medical condition.
o Most cluster A disorders seem to have similarities with schizophrenia, but it is
more long-lasting. Schizophrenia generally is more episodic.
 o Epidemiology: Onset is usually by early adulthood. People are very unlikely to
present for treatment which has implications for prevalence. Prevalence is
estimated to be between 2.3-4% of the population (Grant et al., 2004).
o Aetiology: Research is sparse. It is more common is relatives of those with
schizophrenia, which suggests genetic loading. Low self-esteem and deficits in
emotional and social processing are also implicated in paranoid PD. People
with paranoid PD can find an ecological niche where the disorder works in
favour for them, e.g. someone with paranoid PD would probably do well in the
military, or in detective work.
 Schizoid PD (cluster A):
o Diagnostic criteria (distilled):
 A. Pervasive pattern of detachment from social relationships and
restricted range of expression of emotions in interpersonal settings.
Includes: no desire for close relationships, chooses solitary activities,
little interest in sexual experiences, takes pleasure in few activities,
lacks close friends or confidants, appears indifferent from
praise/criticism, shows emotional coldness/detachment/flattened
affectivity.
 B. Does not occur exclusively during schizophrenia or other disorder w
psychotic features, or medical condition.
o Epidemiology: Onset is early adulthood. Prevalence is 2.2-4% of population
(again not a lot of research).
o Aetiology: Again very little research, there are some that even call for it to be
removed from DSM-5 pre-publication. This is partially due to speculation that
it is linked to Asperger’s. It is associated with a barren upbringing as well as
an underpowered limbic system. A lot of research focuses on upbringing and
parents, but we have to be careful not to blame parents for children having a
PD. There are many other factors at play. This is not associated with
schizophrenia spectrum disorders (despite the name). It is associated with
quite high levels of dysfunction (as are many of the other PDs).
 Schizotypal PD (cluster A):
o Diagnostic criteria (distilled):
 A. Pervasive pattern of social and interpersonal deficits marked by
acute discomfort and reduced capacity for close relationships, as well
as by cognitive/perceptual distortions (psychotic symptoms) and
eccentric behaviour. Includes: ideas of reference, odd beliefs/magical
thinking, unusual perceptual experiences, odd thinking and speech,
suspiciousness/paranoid ideation, inappropriate/constrained affect, odd
or eccentric behaviour or appearance, lack of close friends, social
anxiety related to paranoia.
 B. Does not occur exclusively during schizophrenia or other disorder w
psychotic features, or medical condition. (Important to outline for all 3
Cluster A disorders).
o Epidemiology: Prevalence of 1.5-4.6% of population (not very accurate
estimates due to lack of research).
o Aetiology: This disorder most resembles schizophrenia and there is a link
there; it may be a milder form of schizophrenia. The disorder involves
cognitive abnormalities in attention and memory deficits. It has been
 associated with higher levels of dopamine neurotransmission (Siever & Davis,
2004). There is often crossover with schizophrenia-spectrum disorders.
 Cluster A case example: “Mark attends therapy at the urging of others. He sits where
instructed, erect but listless. When the therapist asks him how he feels about attending
therapy, he shrugs and mumbles ‘OK, I guess’. He rarely twitches or flexes his
muscles or in any way deviates from the posture he has assumed early on. He shows
no feelings when discussing his uneventful childhood, his parents (‘of course I love
them’), and sad and happy moments he recollects at the therapist’s request. Mark
veers between being bored with the encounter and being annoyed by it. When asked
how he would describe his relationships with other people, he states that he has none
that he can think of. In whom does he confide? He eyes the therapist quizzically:
‘confide?’ Who are his friends? Does he have a partner? No. He shares pressing
problems with his mother and sister, he finally remembers. When was the last time he
spoke to them? More than two years ago, he thinks.” This is schizoid PD.
 Antisocial PD (cluster B)
o Diagnostic criteria (distilled):
 A. Pervasive pattern of disregard for and violation of the rights of
others
 Includes (mainly behaviours): failure to conform to social
norms/lawful behaviour (behaviour that is grounds for arrest),
deceitfulness, impulsivity or failure to plan ahead, irritability and
aggressiveness (repeated fights/physical assaults), reckless disregard
for safety, consistent irresponsibility, lack of remorse.
 B. Individual at least 18 years of age. This is important because if you
are diagnosed with similar traits earlier on it may be a conduct disorder
(childhood version of APD).
 C. Evidence of conduct disorder before 15 years.
 D. Does not occur exclusively during schizophrenia/bipolar.
o Epidemiology: Prevalence varies depending on sample. Community samples
about 3%-3.5%. It is over-represented in prison populations
o Aetiology: It is associated with high sensation-seeking, childhood conduct
disorder and low psycho-physiological arousal (presented with distressing
images). It is elevated in family members, as in higher levels of criminality.
The genetic contribution involves impulsivity and is associated with low levels
of serotonin and problems with the frontal lobe. It is associated with high
levels of childhood aggression and with physical abuse, as well as harsh and
neglectful parenting. There is a demonstrated link with psychopathy (but is
actually different to APD, not in DSM-5, APD is focused on behaviour,
psychopathy is more trait-based about lack of empathy and remorse). A
particularly salient question in thinking about this disorder is what should be
the implications for sentencing in a judicial setting? Should they be treated
rather than incarcerated?
 Borderline PD (cluster B): Most well-known and researched
o Diagnostic criteria (distilled): A. Pervasive pattern of instability of
interpersonal relationships, self-image (how can we assess?), and affects,
marked impulsivity. Includes: frantic efforts to avoid abandonment, unstable
and intense interpersonal relationships, identity disturbance (how can we
measure?), impulsivity (e.g., spending, sex, binge eating, reckless driving),
recurrent suicidal behaviour/self-harm, affective instability (marked reactivity
of mood), chronic feelings of emptiness, inappropriate/intense anger, transient
 paranoid ideation. (Mix between behavioural aspects, cognition and
affectivity)
o Epidemiology: Community samples show prevalence rates of 1.6-5.9%. 79%
of BPD diagnoses are females (is this because we are better at detecting it in
females? Are these symptoms just more geared towards women?). Onset is
early adulthood, but recent research shows adolescent diagnosis also has
diagnostic validity and can be quite helpful.
o Aetiology: Torgersen et al. (2000) found a genetic contribution. Meta-analytic
data indicates an association with sexual and physical abuse, parental
hostility/verbal abuse, and neglectful and invalidating environments.
Biologically, increased hippocampal volumes and heightened activation in the
amygdala have been found in BPD patients (this makes sense because emotion
dysregulation is a major component of BPD, and the amygdala is central for
emotions). Research shows patients have insecure attachment and a fear of
abandonment, with a desire for intimacy but intense anxiety about dependence
on others (lots of research on this).
o Comorbidity: High comorbidity with mood disorders, anxiety disorders, and
substance use disorders.
o BPD and suicide: The risk of death by suicide in BPD patients is 45 times
higher than for general population. Review of suicide cases to Coroner’s Court
of Victoria between 2009 – 2013 found: 6.3% of people had a recorded BPD
diagnosis (further 2.5% ‘suspected’). Mental health service contact was made
by 98.9% of those with BPD in 12 months prior to the suicide, 88% 6-weeks
prior. Note that you need service contact to receive a diagnosis. We know that
people with BPD have strong help-seeking behaviour (this is a good thing),
which is different to Cluster A PDs which have inaccurate prevalence rates
because they do not attend treatment. It is often too late, however, and thus
people advocate for earlier diagnosis.
o Some arguments posit that BPD is better defined as a mood/emotional
regulation disorder or a form of PTSD. Cluster analysis revealed a difference
between BPD and complex PTSD (despite overlap) including ‘frantic efforts
to avoid abandonment’, ‘unstable sense of self’, ‘unstable and intense
interpersonal relationships’, and ‘impulsiveness’. BPD also does not respond
to mood stabilising medication as with mood disorders, and treatment for BPD
and complex PTSD also differ.
 Histrionic PD (cluster B): This seems a bit outdated
o Diagnostic criteria (distilled): A. Pervasive pattern of excessive emotionality
and attention seeking. Includes: uncomfortable when not centre of attention,
interaction characterised by inappropriate sexually seductive or provocative
behaviour, rapidly shifting and shallow emotional expression, uses physical
appearance to draw attention to self, speech overly impressionistic and lacking
in detail, is suggestible, considers relationships more intimate than they are.
o Epidemiology: Onset is by adulthood. Prevalence is 0.8-1.8% (potentially due
to lack of research). More commonly diagnosed in females. Is this due to
stereotypes? It potentially should be excluded.
o Aetiology: Little research. Family studies show higher rates of BPD, APD,
and HPD in relative (genetic component). Theoretical accounts focus on
encouragement of sexualisation, attention-seeking and role of intense,
inconsistent and non-empathic parenting interactions.
 Narcissistic PD:
o Diagnostic criteria (distilled): A. Pervasive pattern of grandiosity, need for
admiration, and lack of empathy. Includes: grandiose sense of self-importance,
preoccupied with fantasies of unlimited success, power, brilliance, beauty, or
ideal love, believes they are ‘special’ and can only associated/be understood
by other special/high status people or institutions, requires excessive
admiration, sense of entitlement, interpersonally exploitative (to achieve own
ends), lacks empathy, envious of others, shows arrogant or haughty behaviours
or attitudes.
o Epidemiology: Onset in early adulthood. Grandiosity is not aligned with
reality/actual achievements. Prevalence is estimated to be 1.2-6.2%. The
majority of people diagnosed are male, with rates between 50-75%. This is
likely culturally construed around gender roles, which favour this behaviour in
males. Research shows increase of narcissism in millennials.
o Aetiology: Early childhood experiences are focused on. One model posits that
it arises when the child’s needs for nurturing and affection were not met.
Kernberg says chronically cold caregivers display either indifference or
aggression towards the child. Stone (1993) adds that compensatory beliefs can
arise when a child is exposed to parental indifference. An alternative theory
posits that too much praise in childhood leads to an inflated sense of ego.
Livesley et al. (1993) say that this PD has the highest genetic loading.
o Factor analysis suggests two underlying subtypes of NPD (Wink, 1991): More
research required
 Grandiosity or Overt Narcissism (represented in DSM): associated
with grandiosity, social charm, failure to respond to needs of others,
invulnerability, entitlement, aggression, and dominance.
 Vulnerability/Sensitivity or Covert Narcissism: uses grandiose
behaviour to mask hypersensitivity to criticism, self-doubt, deep
feelings of inadequacy, incompetence, inferiority, worthlessness and
negative affect (high neuroticism). This may present as more
introverted. Targeting these deeper feelings may potentially soften
narcissistic traits.
 Cluster B case example: “A student quickly formed a very intense relationship with
another student she met in class. Immediately, the young woman wanted to spend all
of her free time with the other student and spoke very highly of her new “best friend.”
However, the first time the other student declined an offer to socialize, the young
woman felt intensely afraid and hurt. She suddenly suspected that her new friend was
abandoning her and lashed out at the other student, berating her and accusing her
friend of deserting her. Understandably, the other student ended the relationship.”
This is a case of BPD. People assume self-harm and suicidality will be implicated, but
this is not always the case as seen here.
 Avoidant PD (cluster C): This cluster is less explored. Social anxiety is a similar
diagnosis.
o Diagnostic criteria (distilled): A. Pervasive pattern of social inhibition,
feelings of inadequacy, and hypersensitivity to negative evaluation. Includes:
avoidance of occupational activities with high interpersonal contact due to fear
of criticism, unwilling to get involved with people unless certain of being
liked, restraint in intimate relationships due to fear of being shamed/ridiculed,
preoccupied with social rejection/criticism, inhibited in new social settings,
 views self as inferior/socially inept, reluctant to take personal risks/new
activities.
o Epidemiology: Prevalence of 2.4%. Differences in cultural expectations are
also important to consider (some cultures value these traits).
o Aetiology: Research shows certain traits develop in childhood, with research
showing associations with high restraint, high neuroticism, and shyness in
childhood. There is a higher incidence of avoidant PD in first-degree relatives.
Jorev and Jackson (2004) found schemas (core underlying cognitions) related
to defectiveness and abandonment are present (difficult to change).
 Dependent PD (cluster C):
o Diagnostic criteria (distilled): A. Pervasive and excessive need to be taken
care of, leads to submissive and clinging behaviour and fears of separation.
Includes: difficulty making daily decisions w/out reassurance, need for others
to make decisions for them, difficulty expressing disagreement due to fear of
rejection, difficulty starting things alone, goes to excessive lengths to obtain
nurturance/support, feels uncomfortable/helpless when alone, urgently seeks
another relationship if one ends, preoccupied with fears of being left to take
care of themselves.
o Epidemiology: Less than 1% prevalence.
o Aetiology: Separation anxiety disorder and agoraphobia are more elevated in
family members. It is also associated with high neuroticism and low
extraversion. There is speculation that it is linked with overprotected
attachment and environment; the world is a dangerous place and the schema
involves beliefs that the patient is incompetent to be able to deal with it alone.
 Obsessive compulsive PD (cluster C):
o Diagnostic criteria (distilled): A. Pervasive pattern of preoccupation with
orderliness, perfectionism, mental and interpersonal control, at the expense of
flexibility, openness, and efficiency. Includes: preoccupied with details, rules,
lists, etc, until the point of the activity is lost, perfectionism interfering with
task completion, excessively devoted to work and productivity to the
exclusion of leisure activities/friendships, is overconscientious and inflexible
regarding morality, ethics, or values, hoarding, reluctant to delegate, miserly
spending style (money viewed as something to be hoarded for future
catastrophes), rigidity, and stubbornness. (Some of these may look positive,
but the threshold is impact on functionality).
o Epidemiology: Prevalence is 3.2-7.9%. It is diagnosed twice as often in males.
o Aetiology: Associated with high perfectionism (often in childhood). Millon
and Davis (1996) proposed that the child may have learned to suppress
feelings and perform approved behavioral routines in order to avoid
punishment or disapproval by parental figures. It is different from OCD, as
OCD is axis I. This is potentially a personality style supported by Western
culture.
 Cluster C case example: “Sam presents to therapy encouraged by his partner, who
feels Sam is not prioritising their relationship. Sam states that he loves his partner and
spends time with them watching a movie at home every Saturday night at 8pm. He
gets quite upset if this plan is changed, or if his partner wants to watch a movie on
another night. He understands that his partner wishes they would socialise more with
their friends, but Sam finds it quite difficult to find the time in his busy work schedule
to accommodate this. Prior to living with his partner, Sam lived with his grandmother
 because of the cheap rent, and when moving in with his partner there was significant
conflict due to him wanting to bring all of his childhood possessions into their new
apartment. Despite having a job with regular work hours, Sam often stays back at
work without extra compensation as it tends to take him a lot longer to write a report,
which needs to meet his high standards.” This is an example of OCPD.
 Personality change due to another medical condition: Diagnostic criteria (distilled)
o Persistent personality disturbance that represents change from previous
characteristic personality function
o Evidence change due to direct pathophysiological consequence of another
medical condition
o Not better explained by other mental disorder/occurs exclusively during
delirium
o Disturbance causes clinically significant distress or impairment in functioning
o Types: Labile, disinhibited, aggressive, apathetic, paranoid, other, combined,
unspecified
o Examples include brain tumour and dementia. This is distinct from other PDs,
as they cannot be diagnosed in the presence of another interfering medical
condition.
 Other specified/unspecified personality disorder: PD that causes clinically significant
distress or impairment but does not meet full criteria.
o Other specified: Clinician chooses to communicate the reason criteria are not
met.
o Unspecified: Clinician chooses not to communicate the reason criteria are not
met, or insufficient criteria.
 Some general issues when diagnosing PDs:
o Establishing prevalence over time: Can be really difficult and not a lot of
research.
o Role of gender norms: Changes over time. Some PDs are skewed by gender,
and this may be due to how criteria are written.
o Diagnosis process
o Age requirements: Normally they are not diagnosed unless they are an adult,
but there are exceptions like BPD.
o Impact of cultural background: Changes as well. Some traits are culturally
bound and evaluated.
o Over-shadowing: From other mental health diagnoses, lots of comorbidity so
it is really hard. Diagnosis needs to be long-standing, usually based on
retrospective information.
 Epidemiology of all PDs: How many people meet criteria for at least one PD?
o Australian data: 6.5% prevalence in adults for all PDs (Jackson & Burgess,
2004).
o Best international studies (show higher prevalence): 13% prevalence found in
Oslo, Norway (Torgensen et al., 2001). A meta-analysis of Western countries
found prevalence of 12% (Volkert et al., 2018). A worldwide pooled study
found a prevalence of 8%, 9.5% in high income demographics and 4.3% for
low/middle income (Winsper et al., 2019).
o In mental health settings, we find a 25-40% prevalence rate, which is much
higher (Bank & Silk, 2001).
 PD diagnosis vs PD traits: People may present with ‘traits’ of PDs without meeting
the full criteria for a personality disorder. These traits can still be very important and
 clinical significance. This has led to a progression towards a dimensional approach to
a categorical system. This is needed, as personality lies on a spectrum. We can think
maybe that DSM-5 disorders are one end of this spectrum.
 Dimensional conceptualisations of personality disorders:
o Issues with DSM conceptualisations of PDs:
 Some DSM PD criteria are behaviours, e.g., criminal acts, others are
traits, e.g., emptiness.
 Some DSM PD criteria are harder to assess (identity disturbance) than
others, e.g., impulsivity.
 Some features of PDs are found in other disorders and also in people
without PDs.
 Diagnostic criteria determined by consensus, and not by empirical
evidence and research.
o Alternative DSM-5 Models for Personality Disorders (AMPD): There is a
dimensional (more of a hybrid) model proposed in the DSM-5 appendix,
which focuses on impairments in personality functioning and pathological
personality traits (less behavioural, much more emphasis on functioning). This
includes categories of Antisocial, Avoidant, Borderline, Narcissistic,
Obsessive-compulsive, and Schizotypal PDs (all the others have been
dismissed and we don’t know the rationale). There is also a general diagnosis
of PD (PD-TS).
 Main criteria of AMPD: Criterion A – level of personality functioning
(and level of impairment), measured in domains of self (identity, self-
direction) and interpersonal (empathy, intimacy); Criterion B –
pathological personality traits, measured in five broad trait domains
(negative affectivity, detachment, antagonism, disinhibition,
psychoticism) with 25 specific trait facets (these replicate low levels of
Big 5 form Costa & McCrae’s NEO-PI, gets very complicated);
Criteria C and D – pervasiveness and stability; Criteria E, G, and G –
alternative explanations for personality pathology.
  Example from AMPD: Antisocial Personality Disorder

 AMPD summary: It has a stronger empirical underpinning, in moving

away from the “cluster” framework. Its advantage is its emphasis on
funcitoning. It encourages consideration of multiple areas of
personality variation (5 domains) and assessment of these via a
dimensional lens. We should note that this is still not truly
dimensional, it merely adds a dimensional element to existing
categories.
o Push for dimensional categorisation: Hopwood et al. (2018) argues that there
is no/poor empirical evidence supporting the hypothesis that personality
disorders are categorical. There is low reliability of categories (we don’t really
know what we’re measuring, SCID is unreliable), and substantial
comorbidities. The individual can meet criteria for a category in numerous
ways, suggesting the categories are vague. There is also little treatment
progress, even treatment for BPD is non-specific. They argue the current
system contributes little, and requires change to an empirically supported
conceptualisation.
o How helpful are categories? Are they not useful in a clinical setting?
  Pros: Guide for treatment; Diagnosis can be a relief for the individual,
lead to understanding re: one’s struggles; Can help clinician
understand client too; Ease of communication (clinical, and also useful
for research).
 Cons: Not much evidence, particularly regarding effective treatment;
Can increase stigma as it is viewed as stable and pervasive (hard to
address this stigma). Are we better off addressing these conditions on
the symptom-level (the specific patterns of behaviour – e.g., emotional
regulation skills in BPD)?
o ICD-11 Dimensional Model: The International Classification of Diseases
(ICD) includes mental health section and the ICD-11 published in 2019 moved
from a categorical to dimensional model (Bach & First, 2018).
 There is a focus on impairment of self and interpersonal functioning,
with global assessments. It is then classified according to severity
(mild, moderate, severe). Diagnosis requires one or more prominent
trait qualifiers in: negative affectivity; detachment; dissociality;
disinhibition; anankastia (OCPD). It includes a Borderline Patterns
qualifier. This is quite similar to the DSM AMPD.
 Dimensional classification: Encourages clinicians to consider PDs
from a different lens, and this may have an impact on treatment
selection and development.
 Watts (2019) argues against the inclusion of BPD qualifier, as there is
no evidence yet that this assists with treatment and reduces stigma. He
says, “Patients have regularly reported that being diagnosed with a
personality disorder is the ultimate character slur, leading to realisation
of every worst fear one has about themselves, and often reinforcing
messages from abusers that they are inherently problematic”.
 Aetiology and cognitive models:
o Basic model of PDs: Personality disorders are associated with the experience
of disrupted attachment with primary carers, trauma, neglect, and deprivation.

o Cognitive models:
 Role of maladaptive core beliefs or “schemas” (Beck, Young), e.g.
abandonment, entitlement, unrelenting standards: We can think of
schemas as a filter through which new information is processed, e.g.
we may perceive an ambiguous email as rejection. Each PD is
characterised by specific maladaptive core beliefs (schemas). Schemas
are resistant to change, which leads to the maintenance of
dysfunctional beliefs, emotions and behaviours (Beck & Freeman,
1990).
 Early maladaptive schema in PDs: are highly resistant to change;
associated with high levels of affect; significantly impair functioning.
The individual selectively perceives and distorts information that
confirms the schema and filters out information that disconfirms them.
Emotion, body sensations and behaviours are tied in with cognitions.
  Examples of different types of schema domains (Young):

 Schema perpetuation in PDs: Schema surrender – Individual accepts

schema as true, fully experiences the associated intense emotions and
behaves according to the schema; Schema avoidance – blocks
thoughts, images, feelings that are part of the schema due to distressing
nature (e.g. substance use) or avoids situations that trigger schema (e.g.
relationships); Schema overcompensation – reacts in extreme opposite
to the schema, the underlying schema remains intact but also creates
more problems.
o Dialectical Behaviour Therapy (DBT) model: Has been applied a lot for BPD.
DBT (Linehan) is a model and therapy based on the following: This could be
applied to other pathologies.
 Dysfunctional emotion regulation system is fundamental– part
biological/ part experiential.
 Temperament - high in neuroticism, heightened baseline arousal,
increased intensity of responses to emotional stimuli;
 Child is subjected to drastically invalidating environments, e.g.,
deprivation, neglect, and physical and emotional abuse.
 Additional issues with PDs:
o Ongoing questions:
 What is the role of culture in the development and conceptualisation of
PDs?
 What is the role of gender? Do differences in prevalence represent
diagnostic biases?
 What is the role of the ecological niche? i.e. when the personality type
rewarded by environment.
 Are PDs increasing in prevalence? Or is it increasing recognition? We
do not have good data on this.
 o Stigma: There is a lot of stigma associated with PDs, e.g. BPD is viewed as
difficult in clinical settings. Personality disorders are also viewed as
“egosyntonic” meaning they are a part of who the person is. Understanding
and empathy is vital; the person is just doing their best to get through life the
best way they know how. Aetiology also places emphasis on parental
behaviour, but we need to be careful of blame; most parents are trying their
best given their personal resources.
o Treatment of personality disorders:
 Psychosocial: CBT or variants (Young Schema Therapy, DBT, CAT)
are used and helpful, and this can be group or individual therapy. For
BPD early detection and treatment is valuable.
 Pharmacological: Behaviour traits associated with personality
disorders are associated with neurochemical abnormalities. We do not
know of pharmacological effects for PDs. Nearly all clinical trials have
been with BPD.
 Outcomes: Cluster A – limited evidence-based treatments; Cluster B –
most research (of BPD) with increasing treatment success; Cluster C –
least severe functional impairment with the best outlook.
 Issues: What are we treating? There is also no consensus on how to
measure improvement. Co-morbidity with other disorders also muddies
the waters. Social and interpersonal function often remain impaired
despite treatment. There is a major lack of evidence-based treatments.
o Strengths-based approaches: The current emphasis in mental health is on
categorising individuals according to pathology. It is focused on pathology,
and generates low self-esteem, stigma, poor quality of life, and is considered
chronic. Instead, we should consider focusing on an individual’s attributes that
promote health. Mental health is seen as normal part of human life, and the
focus on individual’s abilities, assets, strengths, allows them to function better
and increase confidence to progress through recovery. The focus is on living
meaningful life despite mental illness. Patients have greater autonomy in
recovery. Strengths-based approaches are associated with better academic,
social, and behavioural outcomes, and increased life satisfaction – but more
research is needed.
 Conclusions:
o PDs cause significant functional challenges for the individual
o There are major issues regarding DSM conceptualisation and assessment.
o Little treatment evidence other than for borderline personality disorder.
o Growing support for dimensional models – and this may facilitate improved
understanding and therefore treatment outcomes.

Prac 5

 Classification of personality disorders:

o Current classification of Personality Disorders: About similarities between
disorders
 Cluster A (odd thinking and eccentric behaviour): Paranoid, schizoid,
schizotypal.
 Cluster B (dramatic and erratic behaviour): Antisocial, borderline,
narcissistic, histrionic
  Cluster C: Obsessive-compulsive, avoidant, dependent.
o Proposed classification of PDs: Measuring impairments in functions or traits.
Self-functioning/interpersonal functioning: This allows us to see how the
disorders are different, allowing for more specified treatment. The DSM
already calls it an “alternative” model.

o Example of how diagnosis would change: Papers are often trying to convince
clinicians to make these more subjective calls.

o Take-away: The process of identifying, classifying, and diagnosing personality

disorders is extremely complex and difficult – no system is perfect. Both the
current model and the proposed model have advantages and disadvantages.
The depth of clinical knowledge required to make a diagnosis is beyond the
scope of this 1.5 hour tutorial – this exercise was for illustrative purposes only.
 Wrapping up:
o Have done all hurdles.
o Exam:
 Format: In-person exam. 90 minutes plus 10 minutes reading time.
You will be permitted to take 1 x double-sided A4 page of notes as a
support to help you transition back to in-person exams! 😃
 Question type: MCQ. Choose the most correct answer (4 options).
  Number of questions: 90 in total. Roughly 10-12 questions from each
of Weeks 5 -12.
 When is the exam? You must check your personal examination
timetable to confirm your exam sitting time. Most but not all students
will sit the exam on June 14. Again, check your personal timetable!
 What is examinable? Anything presented in lectures (including what
was said!), practical classes, assigned readings, and the Week 5
Hearing Voices video.
 Pay attention to readings referred to in pracs.

Lecture 12: Eating Disorders

 Background:
o Commonly held (incorrect) pre-conceptions about EDs: you can tell someone
has an eating disorder by looking at them; someone with an eating disorder
will not be in the “normal” weight range; eating disorders are a choice and
people should just eat more/less.
o What is “normal” eating? It can be difficult to disentangle what is normal and
not, what is healthy and not healthy. Why do we need to label everything as
healthy now? Normal eating can be characterised in many different ways: you
eat when you’re hungry and stop when you’re satisfied; sometimes you just
eat because it feels good; eating is only one important area in your life (it is
not an obsession); you use moderate constraint without being too restrictive;
and you may over-eat at times, or which you had more, and this is normal.
o Eating pathology:

 DSM-5 Feeding and Eating Disorders: Changes have not been super successful,
OSFED (previously Eating Disorder Not Otherwise Specified) is still most prevalent.
o Anorexia Nervosa (AN) (criteria less stringent now)
o Bulimia Nervosa (BN)
o Binge Eating Disorder (BED) (was not part of eating disorders)
o Other Specified Feeding and Eating Disorder (OSFED) (now includes sub-
categories)
o Other Unspecified Feeding and Eating Disorder (new category, not very
common with not a lot of research, wastebasket diagnosis)
o Pica (feeding disorders, added, previously not part of EDs)
o Rumination disorder (added)
o Avoidant/Restrictive Food Intake Disorder (added)
 Anorexia Nervosa:
o Diagnostic Criteria:
  A. Persistent restriction of energy intake leading to low body weight.
(no specification of how low the body weight should be in DSM-5,
was in DSM-IV).
 B. Intense fear of weight gain or persistent behaviour that interferes
with weight gain
 C. Disturbance in how weight/shape is perceived, undue influence of
weight/shape on self-evaluation, or lack of recognition of seriousness
of current low weight
o Subtypes: Very different
 Restricting type (AN-R): Classical anorexia restricting food intake,
counting calories, leading to weight loss (score high on perfectionism)
 Binge eating/purging type (AN-BP): After restriction of intake, access
to food leads to over-eating and binging. It is different from bulimia is
that anorexia binge purging subtypes are underweight. The
personalities are very different as well (score high on impulsivity)
o Epidemiology:
 Sex ratio is 10 females : 1 male.
 12-month prevalence is 0.4%-0.8% (low-occurring disorder, we don’t
have good data particularly for males, probably increased since
pandemic).
 Onset is adolescence to early 20s. We do know of later onset.
 It has a varied course: some experience recovery after a single episode
(early intervention is important); some fluctuate between weight
restoration and relapse; some have chronic course over many years
(quite common, often considered a different subtype); some have
crossover to other EDs (especially BN and binge-purging, the other
way around is much less common).
 Comorbidity: High comorbidity with anxiety and depression (30-60%),
as well as OCD.
o Main features of AN:
 Psychological factors (AN-R): perfectionism (across the board for
EDs); harm avoidance; feelings of ineffectiveness; inflexible thinking;
socially inhibited; overly restrained emotional expression; some
overlap with ASD.
 Clinical presentation: gradually eliminating food; food rituals;
preoccupation with food; ignoring hunger cues; baggy clothes to hide
body.
 AN-BP psychological factors are more similar to Bulimia Nervosa.
 o Physical changes: There are serious physical side effects associated with EDs.
Loss of menses is an important feature, as well as osteoporosis which can
often be longer lasting after eating recovers.

o Health complications: Has cardiac, endocrine (including osteoporosis and

amenorrhea), gastro-intestinal, and many more impacts on these systems.
Frequent hospitalisation is common, and AN has the highest death rate of any
mental health condition.
o Cognitive changes: Mild deficits in executive functioning, memory, verbal &
visuospatial processing can impede recovery – e.g. rigid thinking. These
impacts mostly improve with weight restoration. Cognitive and Health issues
can severely impact adolescent development.
 Bulimia Nervosa:
o Diagnostic criteria:
 A. Recurrent episodes of binge eating (requires criteria of size [much
larger than normal] & time [in about 2 hours] & loss of control)
 B. Recurrent inappropriate compensatory behaviour to prevent weight
gain (e.g., Purging, laxatives/diuretics, fasting, excessive exercise).
 C. Occurs at least once per week for 3 months (in DSM-IV was twice a
week)
 D. Self-evaluation unduly influenced by body shape and weight
 E. Does not occur exclusively during AN episode
 Subtypes: purging (classic vomiting and laxatives) or non-purging
(involves things like fasting, exercise) subtypes (not specified in DSM-
5)
o Epidemiology: Sex ratio is 10 females : 1 male. Prevalence is relatively low of
1-1.5% (not great data, the shame of these disorder probably plays a role).
Onset is late adolescence or early adulthood (usually later than AN). It is often
preceded by AN. It frequently begins during or following an episode of
dieting.
o It has a varied course. It can be chronic or intermittent. For many, it persists
for several years. Periods of remission often alternate with recurrences of
binge eating. Purging can become addictive.
o Has high comorbidity with depression and anxiety, as well as substance use
(impulsive psychopathologies).
 o Clinical presentation: binge-purge cycle; preoccupation with food; recognition
that the behaviour is maladaptive; weight is typically in average range.
Psychological factors include low self-esteem and guilt, as well as impulsivity.
It is a vicious cycle that can be very difficult to break.

o See diagram above for physical changes of bulimia. It can result in death as
these symptoms affect the heart.
 Binge Eating Disorder (BED): First time it has its own diagnosis, used to be part of
EDNOS.
o Diagnostic criteria:
 A. Recurrent binge eating (same criteria of size + time + loss of
control)
 B. Three or more of the following: Eating more rapidly than normal;
Eating until uncomfortably full; Eating large amount of food when not
hungry; Eating alone because embarrassed or disgusted; Depressed or
guilty after over-eating
 C. Marked distress regarding binge eating
 D. Occurs once per week, 3 months +
 E. No regular use of inappropriate compensatory behaviours
o Prevalence: Higher prevalence than bulimia of 2-3%. The gender difference is
less skewed. Prevalence is also higher in very overweight populations.
o Clinical features: guilt and shame regarding binging behaviour, secrecy; eating
when not hungry; eating for emotional control. It is associated with increased
psychological distress and metabolic disturbance.
 DSM-5 Severity Indexes: No established research that validates these cut-offs, they
have been chosen fairly arbitrarily. Research shows they are not that predictive.
o Anorexia Nervosa (BMI):
 Mild: BMI of ≥ 17 kg/m2
 Moderate: BMI of 16-16.99 kg/m2
 Severe: BMI of 15-15.99 kg/m2
 Extreme: BMI ≤ 15kg/m2
o Bulimia Nervosa (frequency of weekly inappropriate compensatory
behaviours):
 Mild: 1-3
  Moderate: 4-7
 Severe: 8-13
 Extreme: >14
o BED has the same thresholds as BN, but only for binge eating episodes.
o Krug, Dang et al. (2020) conducted a study on severity indexes: Bottom shows
transdiagnostic severity index, looking at “drive for thinness”. Note how DT is
much higher for BN.

 Other Specified Feeding or Eating Disorder (OSFED): Very little research and is a
huge mixed bag. It is defined as clinically significant distress or impairment that does
not meet full criteria for another disorder. DSM-5 has tried to separate out the
different OSFEDs and give some examples:
o Atypical Anorexia Nervosa: All criteria are met, except despite significant
weight loss, the individual’s weight is within or above the normal range. Has
similar health consequences, impairment, and comorbidities to AN. This is
harder to detect as the person does not present as ‘underweight’. There is no
specialised treatment, and more research is needed.
o Purging Disorder (PD): Recurrent purging behaviour to influence weight or
shape in the absence of binge eating.
o Night Eating Syndrome: Recurrent episodes of night eating. Characterised by
eating after awakening from sleep, or by excessive food consumption after the
evening meal.
o Subthreshold BN (e.g. sporadic purging/binging)
o Subthreshold BED
 Purging Disorder: Proposed definitions and studies
o Definition: Purging episodes (e.g., self-induced vomiting, laxative and/or
diuretic misuse) in the absence of objectively large binge-eating episodes to
control their weight or shape. Must have occurred at least once a week over
the past 3 months. BMI needs to be >18.5 (Keel et al., 2007; Keel, 2019).
 o The “objectively large” (much larger than normal) is important, as there are
people engaging in subjective binge eating (often the case in AN). People may
think they have a binge, but it is actually just a normal meal portion.
Subjective binges can trigger many of the same cognitive symptoms,
nevertheless, and it is very hard to measure. Can often require education about
normal meal sizes. Also needs to be a loss of control overeating. There aspects
are not that well defined.
o Cluster analysis of Purging Disorder (Krug et al., 2020): n = 223. Found 3
clusters.

o Distribution of PD clusters based on DSM-5 severity index for BN (Ibid.):

Cluster 3 is most severe, and significantly more so. The number of purging
methods could be considered as an alternative severity index. Very little
research looking at this.
 Unspecified Feeding and Eating Disorder: Again, it is clinically significant distress or
impairment that does not meet full criteria for other disorder. It is used when the
clinician chooses not to specify why criteria are not met, or in presentation where
there may be insufficient information to make a more specific diagnosis (e.g. in
emergency room settings). This isn’t that helpful.
 Avoidant Restrictive Food Intake Disorder (ARFID)(feeding disorder):
o Diagnostic criteria:
 A. Persistent failure to meet appropriate nutritional and/or energy
needs associated with one or more of the following: significant loss of
weight (or failure to achieve expected weight gain or faltering growth
in children); significant nutritional deficiency; dependence on enteral
feeding or oral nutritional supplements; marked interference with
psychosocial functioning.
 B. Not better explained by lack of available food or by an associated
culturally sanctioned practice.
 C. The behaviour does not occur exclusively during the course of AN
or BN, and there is no evidence of disturbance in the way one’s body
weight or shape is experienced.
 D. The eating disturbance is not attributed to a medical condition, or
better explained by another mental health disorder.
o Epidemiology: Age of onset is younger than AN/BN, usually in childhood. It
is associated with: childhood picky eating; generalised anxiety;
 gastrointestinal symptoms; comorbid medical conditions; less likely to have a
mood disorder than AN or BN. It is slightly more common in males (very
different to eating disorders).
 Pica: Criteria
o A. Persistent eating of nonfood substances for a period of at least 1 month
o B. The eating of nonfood substances is inappropriate to the developmental
level of the individual.
o C. The eating behaviour is not part of a culturally supported or socially
normative practice.
o D. If occurring in the presence of another mental health disorder (e.g. ASD),
or during a medical condition (e.g. pregnancy), it is severe enough to warrant
independent clinical attention.
o Prevalence data yet to be established, but appears to be more common in those
with an intellectual disability. Increased prevalence in pregnancy.
 Rumination disorder: Criteria
o A. Repeated regurgitation of food for a period of at least one month.
Regurgitated food may be re-chewed, re-swallowed, or spit out.
o B. The repeated regurgitation is not due to a medication condition (e.g.
gastrointestinal condition).
o C. The behaviour does not occur exclusively in the course of AN, BN, BED,
or ARFID.
o D. If occurring in the presence of another mental health disorder (e.g.neuro-
developmental disorder), it is severe enough to warrant independent clinical
attention.
o Prevalence data yet to be established, appears to be more common in those
with an intellectual disability.
 Also consider Disordered Eating: this is subthreshold eating pathology (not in DSM-
5). It is very common in adolescents (16.3% estimate in Australian samples). It is
associated with psychosocial impairment and comorbid psychopathology. This is
often a precursor to a full-blown ED.
 Also consider Orthorexia: Not an official DSM-5 diagnosis, may start as “clean
eating”, and progresses to the elimination of many food groups. It is characterised by
inflexible eating behaviours aimed at “purity”. Emotional wellbeing becomes overly
dependent on eating the “right” foods.
o This has similarities to AN: health risks/malnutrition form cutting foods; rigid
food rules and preoccupation with food; interference with normal functioning.
o Has been reasonably recently detected. It raises the question of the impact of
media/culture on psychopathology?
o There could be a long discussion of when “clean eating” becomes unhealthy.
This would probably be when it impacts on functioning. Food itself can’t be
“healthy” or “unhealthy”, good or bad, it is about our relationship to it and the
variation in our diet.
 Also consider Muscle Dysmorphia: This is not an Ed but has a substantial body image
component. It is a subtype of Body Dysmorphic Disorder. It has been termed
“bigorexia” and is comparable to an AN body image disturbance. It is a preoccupation
regarding a subjective lack of muscularity. They genuinely see themselves as smaller
and this can lead to disordered eating (e.g. drastically increasing protein and
decreasing fats). This mostly affects males.
 Transdiagnostic and symptom-level models:
o Diagnostic overlap: Classification of main ED subtypes according to the
DSM-5 (APA, 2013).

o Diagnostic instability (Krug et al., in prep.). Graph below shows crossover of

different EDs. 34.5% of patients had a stable ED.

o Transdiagnostic model of EDs: Motivated by the prevalence of crossover. This

model is proposed by Fairburn (2003). Model has manualised treatment which
is very effective. Can be applied to any eating disorder with some
specifications. All EDs have this “dysfunctional scheme for self-evaluation”.
The clinician can choose whether to use these specification modules for things
 like low self-esteem, interpersonal problems, and mood intolerance.

o This model shows the mechanism explaining why restriction often leads to
binging. Strict dieting and weight control behaviour can lead into “starvation
syndrome” (AN) or binge/purging symptomatology (BN, BED).
 Aetiology of Eating Dosorders:
o DSM-5 categories are still important. We need research that informs DSM
diagnosis, and DSM diagnosis also informs the research. This interaction
informs treatment.
o Risk factors and correlates for EDs:
 Risk factors from cohort-based longitudinal studies: dieting (#1 risk
factor); personality factors (neuroticism, negative affect, perfectionism
for AN); body dissatisfaction; thin-ideal internalisation and social
pressure to be thin; perinatal factors, including premature birth and
complications during delivery; parental psychiatric factors; genetic
factors.
 Numerous correlates (i.e. from cross-sectional studies) have been
identified, including childhood abuse, certain family environments, and
weight-based criticism.
o Gender:
 Being female is a big risk factor for EDs, but males are likely under-
represented.
 Eating disorders in males: The average age of onset is later than for
females. Diagnoses are associated with jobs requiring a particular body
look or exercise regimen. Muscularity is more likely to be a focus.
Dieting is a less common risk factor for men. 15% of gay or bisexual
men have struggled with EDs, and around 42% of men with an ED
identify as gay or bisexual.
 Transgender and gender non-binary populations: There is limited
research so far. Early evidence suggests a greater risk for this
demographic. Food restriction may be related to preventing puberty
onset/progression.
o Insights from twin studies: These are all factors implicated in EDs. We have
found that “non-shared environment” is the most important for EDs (may also
 apply to other mental health problems. Genetics are also quite important.

o Role of genetics:
 Eating disorders aggregate in families: heritability estimates are around
40-60% (quite high). Biology is involved, not as much as
schizophrenia or autism, but is still important.
 Candidate gene studies (e.g. serotonin transporter gene) looks at a
specific gene, and whether it is expressed more commonly in an ED
population than in control. We know that we have thousands of genes,
so assessing one is a bit arbitrary.
 Genome Wide Association Study (GWAS): This is actually quite
outdated now. 5 have been conducted so far, all for AN. This assesses
the whole human genome. These identified several risk loci, also
associated with psychological traits (OCD) and metabolic factors.
Studies have been conducted mostly in European countries. Taking
ancestry into consideration is important.
 Gene-environment interactions: Looks at the combination of genetic
susceptibility and environmental factors. They suggest the environment
is very important. This had to be conducted with the candidate gene
studies initially. Caspi did the first version of this study for anxiety and
depression (well-cited). EDs do not have much data in this area, it is
difficult to get a sample. It is usually to do with maladaptive
environments (abuse, other stressful life events), and they mainly focus
on serotonin transporter gene as well, as this has been implicated.
Rozenblat et al. (2017) conducted a meta-study that summarises the
results of these studies. Found gene-environment interactions with
stressful life events, and also looked at plasticity, whether positive
environments make people less likely to develop illness. No results
here.
o Eating disorders around the world: They are a Westernised disorder, as shown
below, with higher prevalence. This may be due to density of research.

o Media and social media: A very important factor nowadays in mental health.
Cultural pressures usually glorify the idea of the “perfect” body. This places
value on people on the basis of physical appearance, not inner qualities and
strengths. Definitions of beauty are narrow for both men and women. The
“desired” body type is constantly changing over time, and this is reflected in
eating pathology. We can see very clearly how different historic beauty ideals
can be. E.g. for males, we can look at G. I. Joe – in 1970 he was 5’ 10” with a
32 inch waist and 12 inch upper arms, by 2000 he had a 29 inch waist and 16.5
inch arms. Same kind of things with Barbie.
o Example of social media trend: Fitspiration and eating pathology.
‘Fitspiration’ (also known as ‘fitspo’) aims to inspire individuals to exercise
and be healthy, but emerging research indicates exposure can negatively
impact body image (Holland & Tiggman, 2017).
 Thinspiration vs fitspiration: “Thinspiration” is aimed at promoting
weight loss and glorifying disordered eating. This has been around for
a while. Fitspiration (more novel) aims to promote fit and healthy
lifestyles. However, fitspiration is also idealising the extremely thin
body, just now with an additional emphasis on muscle tone. This is
related to body dissatisfaction, negative mood and disordered eating.
 Experimental EMA design to assess fitspiration: Looks at impacts of
these images, exposing individuals to these images. 60 images (30
fitspiration and 30 neutral) were piloted amongst 60 male participants.
Highest scoring 15 fitspiration images & 15 neutral images (furniture,
plants, art) from Instagram were selected from the pilot phase to be
included into the instant survey app. Participants received signalling of
images at random intervals 5 times per day, every day for 7 days.
There were a total of 35 assessments over the entire Phase 2 period.
People were randomly assigned to view fitspiration or neutral images.
 There were asked before and after viewing the images to rate pressures
to change body image, satisfaction variables, and disordered eating.
Krug et al. (2021) did not find significant findings in females. Yee et
al. (2021) found much more significant findings (was a better-quality
study).
 Male fitspo/thinspo study overview of findings (Yee et al., 2021):
State-based data before ad after images. Viewing fitspiration images:
increased body fat dissatisfaction (d = 0.12); increase in muscularity
dissatisfaction (d = 0.14); increase in negative mood (d = 0.11);
increased urge to engage in behaviours to reduce body fat (d = 0.06);
increased urge to engage in behaviours to increase muscularity (d =
0.11). These were the more significant effects. Viewing thinspiration
images: decreased body fat dissatisfaction (d = -0.05); decreased
muscularity dissatisfaction (d = -0.09); increased negative mood (d =
0.05); found no change in the urge to engage in behaviours to reduce
body fat (d = 0); increased urge to engage in behaviours to increase
muscularity (d = 0.05). Fitspiration is more negative in the male
population.
 Thankfully, there is growing resistance to these trends. The Body Shop
has done some amazing campaigns. Bodies can come in all shapes and
sizes.
o EDs and COVID: We saw an increase in prevalence and symptom severity.
Lockdowns generally had a negative impact on mental health, creating
boredom and anxiety (however meta-analytic evidence is mixed). People had
access to food at home at all times, and there was restriction on exercise (gyms
closing). This time at home led to greater social media exposure, a risk factor
ED. Social isolation is another important risk factor of EDs, and exposure to
depressing news led to increases in comorbidity.
o Dual pathway model of BN (Stice, 2001): Combines risk factors into a path
model. There is decent support for this model. The two parts of the “dual”
pathway are binge eating as a result of restriction (“dietary restraint”) and
binge eating as an emotional regulation technique (“negative affect”):

 Most studies conducted in support of this model are cross-sectional.

Only very few longitudinal studies have used SEM to assess the model,
controlling for temporal stability of bulimic pathology.
 Cross-sectional studies: Have around 50% variance (not that high).
There is a question that emerges from these studies about the role of
dietary restraint.
  Longitudinal studies: Have around 30-54% variance. For these studies,
all hypothesised paths were supported (methodologically more sound).
 Theoretical limitation: DPM accounts for around 54% variance, which
suggest other factors need considering, like personality. DPM cannot
account for why sociocultural factors only impact some people.
o Tripartite Influence Model for Eating Pathology (Thompson et al., 1999):
Quite similar to previous model, but differentiates different influences.
Evidence: Cross-sectional, e.g. Huxley et al., 2015; Javier et al.,, 2015; Shroff
et al., 2006; Schaefer et al., 2014; Longitudinal, e.g. Rodgers, Paxton &
McLean, 2014.

o An aetiological model of EDs:

 o A more complex aetiological model: This was lecturer’s PhD.

 Treatment outcomes and approaches:

o Evidence based treatment (Nazar et al., 2017):
 This is gradually increasing for specific treatments. For example,
family-based treatment has been shown to be effective for AN in
adolescents (gold standard), and CBT/CBT-E and guided self-help has
been effective in treating BN and binge eating.
 Early symptom improvement is predictive of better outcomes long
term, so it is important to get into treatment quickly.
 ED research is still in its infancy (like most mental health disorders),
but this does not mean that treatment doesn’t work. EDs are unlikely to
spontaneously recover without treatment. It can involve inpatient, day
program, or weekly individual therapy.
o Barriers in recovery from EDs (Gregertsen et al., 2017):
 Many don’t seek treatment: they don’t recognise the seriousness of
condition (may even think that it gives them benefits); the ED may
even be encouraged by friends and family – but there is often secrecy;
people are fearful of change associated with recovery; and EDs are
usually egosyntonic, it becomes part of who they are.
 Very low BMI often requires inpatient admission
 Behaviours can become deeply ingrained. They can be very hard to
change.
 Early Behaviour Programs (EBP) often involves targeting behaviours
early, followed by addressing body image and related factors
(cognitive).
o Emerging approaches:
 ‘Health at every size’ movement: We have limited control of our body
shape/weight in the long term. Being ‘overweight’ does not necessarily
equate to ‘unhealthy’. This involves addressing weight stigma in the
medical field.
 Body positivity: Aims to embrace diversity and the uniqueness of your
body. This fights against the ‘thin ideal’, and advocates for body
neutrality.