Download The Abnormal Psychology option

ABNORMAL PSYCHOLOGY
The Abnormal Psychology option
1. General framework
A. The influences of biological, cognitive and sociocultural factors on abnormal behaviour.
B. Evaluation of psychological theories and/or studies relevant to the study of abnormal behaviour.
2. Concepts and diagnosis
A. Normality and abnormality
B. Validity and reliability of diagnosis
C. Cultural and ethical considerations in diagnosis
3. Psychological disorders
A.
i.
ii.
iii.
Symptoms and prevalence
Affective disorders (major depressive disorder)
Anxiety disorders (post-traumatic stress disorder)
Eating disorders (bulimia nervosa)
B.
i.
ii.
iii.
Etiologies (biological, cognitive and sociocultural factors)
Affective disorders (major depressive disorder)
Anxiety disorders (post-traumatic stress disorder)
Eating disorders (bulimia nervosa)
4. Implementing treatment
A.
i.
ii.
iii.
iv.
Therapeutic approaches to treatment
Biomedical
Individual
Group
Eclectic
B. The relationship between etiology and therapeutic approach
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1. General framework
A. The influences of biological, cognitive and sociocultural factors on abnormal
behaviour.
Abnormal psychology focuses on diagnosing, explaining and treating humans suffering from
psychological disorders. The first step to this is examining to what extent different factors influence
abnormal behaviour. Psychologists working at different levels of analysis will have different opinions
and beliefs about the relative influence of either the biological, cognitive or sociocultural factors,
though all would agree that it is often an interaction of all three that affect abnormal behaviour.
Of issues relate
Learning outcome:
To what extent do biological, cognitive and sociocultural factors influence abnormal
behaviour?
Biological factors
The main principles of the BLOA are:
•
•
•
Patterns of behaviour can be inherited.
There are biological correlates to behaviour.
Non-human animal research may inform our understanding of human
behaviour.
Therefore, psychologists or psychiatrists* looking for biological factors
will look at the role of inheritance in abnormal behaviour, will explore
brain structure and functioning to see if this is related to abnormal
behaviour, and will examine animal research into abnormal behaviour to
see if the results can inform us about human abnormal behaviour.
(*psychiatrists are trained as medical doctors and then study a speciality in psychiatry.
Psychologists usually have a post-graduate degree in clinical psychology. Psychiatrists may
prescribe medication; psychologists may not.)
Study into biological factors and abnormal behaviour
Avena (2007) investigated the role of neurochemicals in binge eating and drug abuse. Binge
eating is one of the behaviours associated with bulimia. The increase in the incidence of eating
disorders has encouraged research efforts aimed at understanding their etiology. Clinical reports
have led to the suggestion that some individuals may develop addictive-like behaviours when
consuming palatable foods.
Avena reviewed the behavioural and neurochemical similarities between the binge eating of food
and the administration of drugs of abuse. An animal model of bingeing on sugar was used to
illustrate behaviours found with some drugs of abuse, such as withdrawal symptoms and higher
intake following abstinence. Related neurochemical changes commonly observed with drugs of
abuse, including changes in dopamine and acetylcholine release can also be found with bingeing
on sugar. These neurochemical alterations are even stronger when animals binge on sugar while
at a low body weight or when the food they take in is later purged. (In humans this would
correspond to lightweight people binge-eating sugary foods and then taking laxatives or vomiting
to empty their stomach). Drawing on other animal models and the clinical literature, parallels
between drug abuse and binge-eating behaviour are discussed.
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Principles that this study could be used to demonstrate
There are biological correlates to behaviour.
Non-human animal research may inform our understanding of human behaviour.
Cognitive factors
The main principles of the CLOA are:
•
•
•
Mental representations guide behaviour.
Mental processes can be studied scientifically.
Cognitive processes are influenced by social and cultural factors.
Therefore, psychologists explaining abnormal behaviour by examining cognitive factors will look at
faulty schemas (mental representations), types of thinking and beliefs (mental processes) and how
these are influenced by social and cultural factors.
Study into cognitive factors and abnormal behaviour
Haeffel and Hames (2013) investigated the role of cognitive vulnerability* and depression.
Cognitive vulnerability is a potent risk factor for depression. Individual differences in cognitive
vulnerability solidify in early adolescence and remain stable throughout the life span. However,
stability does not mean never changing. The researchers investigated whether cognitive
vulnerability was susceptible to change during major life transitions such as moving to college.
They tested the hypothesis that cognitive vulnerability could change according to a person’s close
companions, by conducting a longitudinal study with a sample of randomly assigned college
roommate pairs (103 pairs). Results supported the hypotheses. Participants who were randomly
assigned to a roommate with high levels of cognitive vulnerability were likely to “catch” their
roommate’s cognitive style and develop higher levels of cognitive vulnerability. Moreover, those
who experienced an increase in cognitive vulnerability also had significantly greater levels of
depressive symptoms over the duration of the study than those who did not.
This study not only shows the effect of cognitive factors on abnormal behaviour, but how cognitive
vulnerability can be transmitted and thus acts as a social factor with regard to depression.
*an outlook on life where you feel like everything is out of your control, and everything bad is in
some way your fault
Principles that this study could be used to demonstrate
Mental representations guide behaviour.
Cognitive processes are influenced by social and cultural factors.
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Sociocultural factors
The main principles of the SCLOA are:
•
•
•
•
Human beings are social animals with a basic need to “belong”.
Culture (social norms and values) influences behaviour.
Because humans are social animals, they have a social self.
People’s views of the world are resistant to change.
Therefore, psychologists explaining abnormal behaviour by examining
sociocultural factors will look at people’s social needs, how their culture
affects what is defined as normal and abnormal and how this influences
their behaviour and the whole process of labelling and being labelled.
Study into sociocultural factors and abnormal behaviour
Chaudry et al. (2011) researched depression in British Pakistani women. The aim of this study was
to determine the relative importance of life events, chronic social difficulties and acculturation
(adapting to the local British culture) in a population-based sample of British Pakistani women.
A longitudinal study of 18- to 65-year-old Pakistani women in UK was carried out. The Schedule
for Clinical Assessment in Neuropsychiatry for diagnosis, the Life Events and Difficulties Schedule
for social stress and an acculturation questionnaire were used.
It was found that depressive disorder at the beginning of the study was associated with older age,
social isolation and marked difficulties involving health and close relationships. Depressive
disorder at follow-up was associated with severity of depression at baseline, difficulties in close
relationships and two aspects of acculturation, especially less acculturation in relation to use of the
English language.
The researchers concluded that a lack of acculturation, especially less familiarity with the English
language, is a predictor of persistence of depression in Pakistani women in UK. This needs to be
taken into consideration when planning treatment, which also needs to address the personal
difficulties associated with persistent depression. The implication of this work is that women of
Pakistani origin with depression should be encouraged to receive help in the use of English as one
part of treatment that may prevent relapse.
Principle that this study could be used to demonstrate
Cognitive processes are influenced by social and cultural factors.
Human beings are social animals with a basic need to “belong”.
(Note: one of these is from the CLOA and one from the SCLOA)
All of these studies take a different approach to researching abnormal behaviour. However, many
psychologists are now working together in a combined approach, as an abnormal behaviour that has
biological correlates can also be maintained by negative thinking and poor social conditions, so it
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makes sense to look at all of three levels of analysis. See this article for an example of how a
combination of approaches is being taken with both analysing the etiology of and treating eating
disorders.
B. Evaluation of psychological theories and/or studies relevant to the study of
abnormal behaviour.
Learning outcome:
Evaluate psychological research (that is, theories and/or studies) relevant to the study of abnormal
behaviour.
Like all research, research related to the study of abnormal behaviour
is subject to evaluation. There are many mnemonics given for
evaluation. Here are two:
MAGEC = methodological considerations, alternative arguments,
gender considerations, ethical and cultural considerations
SECRET G = Sampling, ethics, credibility, reflexivity, expectations/bias, triangulation and
generalizability. (Especially useful for questions on qualitative research methods, at HL).
But, the important thing is that the evaluation must be made relevant to the question, and must use
the command term, which might be “evaluate” but equally well might be “discuss” or “to what
extent?” or any of the other Level 3 command terms (see the Psychology guide, p 17)
A study into abnormal behaviour and a published review (evaluation) of the same study
Study. Bach and Hayes (2002) examined the impact of a brief version of an acceptance-based
treatment (acceptance and commitment therapy; ACT) that teaches patients to accept unavoidable
private events; to identify and focus on actions directed toward valued goals; and to defuse from
odd cognition, just noticing abnormal thoughts rather than treating them as either true or false.
Eighty inpatient participants with positive psychotic symptoms were randomly assigned to
treatment as usual (TAU) or to 4 sessions of ACT plus TAU. ACT participants showed significantly
higher symptom reporting and lower symptom believability (they did not believe their abnormal
thoughts), and a rate of rehospitalisation half that of TAU participants over a 4-month follow-up
period. The same basic pattern of results was seen with all participant subgroups except
delusional participants who denied symptoms.
(However, see the review of this study, below. If you quote this study at all, you should also
mention the review and criticisms by Coyne, 2011).
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A published review (evaluation) of Bach and Hayes’ study
Review. Coyne (2011) wrote in his Psychology Today blog that the researchers were not justified
in concluding that a brief Acceptance and Commitment Therapy (ACT) intervention reduced
rehospitalisation of psychotic patients by one half. The simple differences in rehospitalisation
between patients receiving the intervention and those in treatment as usual (TAU) were not
significant. The "one half" statistic was misleading, particularly when patients who killed
themselves or went to jail rather than being rehospitalized are taken into account.
Coyne argued that
1. We cannot confidently determine that rehospitalisation was set as the primary outcome of
the trial before data collection actually began.
2. At least 40 patients were assigned to each group, not the 35 on whom analyses were
conducted. Patients were dropped from the analyses that had negative outcomes arguably
as bad as rehospitalisation-- suicide and going to jail. If a patient committed suicide, rather
than getting rehospitalized, it can hardly be considered a positive outcome.
3. We don't know whether the treatment as usual provided to the control patients was even
adequate or whether the ACT patients got more of this treatment than the TAU patients.
He concluded that the abstract is not an accurate guide to actually happens in the study.
“The abstract says a rate of rehospitalisation half that of TAU over a four-month follow-up, but the
differences of 7/35 patients rehospitalized in the ACT group versus 14/35 patients in the TAU is
not significant. Moreover, it is noteworthy that there were 40 patients assigned to each group, not
the 35 that were analysed.”
He is criticising this research on both its accuracy and its ethics. It could be argued to be unethical
to promote a treatment (ACT) that actually resulted in the reporting of more symptoms, and the
abstract does not reflect accurately what is in the article. The sample was small, and people were
excluded if they had negative outcomes.
Principle that this study could be used to demonstrate
Mental representations guide behaviour.
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While you will mainly be reading reports of studies in textbooks, though you will read some original
studies, look out for what is not said, as well as what is said. For example what gender were the
participants? What age were the participants? What ethnicity were the participants? Were they all
university students? Were they all psychology students? Could we have expected the same results
if the study had used real-life situations instead of laboratory ones? Be a detective.
Reports published in newspapers are particularly suspect and should be tracked back to their
original source. See this news article for an example of researcher bias. Who conducted the study?
What do they sell?
2. Concepts and diagnosis
It is much more difficult to diagnose abnormal behaviour and further
identify it as a symptom of a mental disorder than it is to diagnose a
physical disorder, where what is under examination is a disorder of the
body rather than one of emotions, thought and behaviour. Mental
health professionals face challenges in the area of defining normality
and abnormality, identifying if a diagnosis is reliable and valid and
considering cultural and ethical issues with diagnosing an individual with a mental disorder. This is
when a comparison and combination of both emic and etic approaches can lead to a greater
understanding.
A. Normality and abnormality
Learning outcome:
Examine the concepts of normality and abnormality.
“Abnormal” is usually taken to mean “deviating from what is normal or
usual”. But this then raises the question of what is “normal”. Each
cannot be defined without defining the other. And the problem with
normal behaviour is that it relies on specific social and cultural norms
that are socially constructed and mutually agreed but vary from place to
place. When we are born and raised in a particular culture, we
internalize the norms and accept them (with the occasional protest), but
understanding the norms of another culture can present problems. For
example, as Wakefield (2007) points out, inability to learn to read due
to a dysfunction in the corpus callosum (assuming that this theory of some forms of dyslexia is
correct) is harmful in literate societies, but not harmful in preliterate societies, where reading is not a
skill that is taught or valued, and thus not a disorder in those societies.
There is also an historical perspective to this, as what is normal also varies with time as well as
th
place. In 19 century Europe and the USA, psychiatrists believed that both physical and mental
activity could be harmful to women. A common diagnosis for women was “hysteria,” a general term
that could be applied to almost any woman. A common “cure” for hysteria was bed rest, preventing
both physical and mental activity. The diagnosis of hysteria (the word comes from the Latin name for
the womb) served as a justification for severely limiting women’s activities. Charlotte Perkins
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Gilman wrote the classic short story “The Yellow Wallpaper” after her own experience of being
forced to stay in bed with no mental stimulation, not even books.
As David Rosenhan writes (1973, p 250)
To raise questions regarding normality and abnormality is in no way to question the fact that some
behaviours are deviant or odd. Murder is deviant. So, too, are hallucinations. Nor does raising such
questions deny the existence of the personal anguish that is often associated with mental illness.
Anxiety and depression exist.
Psychological suffering exists. But normality and abnormality, sanity and insanity, and the diagnoses
that flow from them may be less substantive than many believe them to be.
Faced with these context-specific concepts of normality and abnormality, in order to diagnose
abnormal behaviour, mental health professionals use several different ways of defining abnormal.
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Statistical infrequency
This is deviation from the average: statistically rare behaviour becomes defined as “abnormal”. One
example might be autism, which only occurs in between 1 and 2% of children in Asia, Europe and
North America (Centre for Disease Control, accessed August 2013). One problem here is that
behaviour may be statistically rare, such as the ability to speak more than five or six languages
fluently, without being a sign of a mental disorder. Other questions are how rare behaviour has to
be before being defined as abnormal, and what about disorders like phobias that are statistically
very common? Clearly more is needed.
Deviation from social norms.
This is a socially-based definition, as the name “social norms” makes clear. If someone continually
breaks these unwritten rules of society, by invading personal space or dressing and acting
inappropriately, for example, then s/he is labelled “abnormal”. (See Rosenhan and Seligman, 1989).
This means it is relatively easy to class someone as “abnormal”, so people may use this as a way of
getting rid of people of don’t conform to a certain view. For example, throughout the mid to late 20th
century many Eastern European countries put people who didn’t agree with the government to
mental institutions, saying they were “abnormal” for not agreeing with their own social norms. (See
writing by Aleksandr Solzhenitsyn).
Moreover, acting in a certain way in one situation or context could be normal, but seen as
completely crazy in another. For example, wearing beach clothes at a beach or swimming pool is
normal, but in a formal occasion it would be a deviance from social norms. So this definition can’t
completely define abnormality as in some situations otherwise abnormal behaviour is quite OK.
Homosexuality and transsexuality occupy a culturally relative position on whether or not they are
normal. In some cultures, both are illegal and punishable by imprisonment; in others, both are
unremarkable. In 1973 homosexuality was removed from the DSM-II classification. (DSM
=Diagnostic and Statistical Manual of Mental Disorders, used by mental health professionals to
classify abnormal behaviour). It was replaced by the category Sexual Orientation Disturbance. This
represented a compromise between the view that preferential homosexuality is invariably a mental
disorder and the view that it is merely a normal sexual variant. If you were homosexual and
disturbed by this, then you had a mental disorder.
A similar change can now be seen with the newly-published DSM 5 and transgender people:
transgender identity was classified as Gender Identity Disorder, and had been labelled as such
since the third edition of the DSM published in the 1980s. Now it is called “gender dysphoria”, which
broadly identifies distress over “a marked incongruence between one’s experienced/expressed
gender and assigned gender.” So, again, it is distress created by the difference between your
expressed and your birth gender that is the problem.
Nonetheless, the DSM 5 is published by the American Psychiatric Association and is not used
worldwide, though it is used widely. Just because a disorder is removed from the manual does not
mean that the behaviour seen as normal in many cultures. (See the argument by Szasz in your
textbook, and here is a controversial interview with him, shortly before he died last year).
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Failure to function adequately
Everyone has difficulties in coping with the world sometimes, but if an
individual’s behaviour, mood or thinking affects their well-being by
making life unbearable, making it impossible to keep a job or have
friends, then the behaviour is seen as abnormal. It is a question of
degree: a heavy smoker or drinker is not necessarily seen as engaging
in abnormal behaviour, even though they are self-harming and may
alienate their friends and have difficulty at work. These are examples of behaviour that have
become less acceptable in recent years.
This definition relies on the judgement of others. The person, who is not functioning adequately, may
feel that s/he is absolutely fine. People who live alone and have few friends or relatives may
therefore not be functioning adequately for much longer periods than those in more social
surroundings before being judged as abnormal. The issue becomes how much the person’s
abnormal behaviour is adversely affecting or threatening others, and how judgemental they are.
Wakefield (2007, mentioned earlier) proposes a model of “harmful dysfunction” for the diagnosis of
mental disorder – a behaviour should be negatively valued both by the community and the individual
(harmful) and also due to the malfunction of some internal mechanism (dysfunction). While the first
of these might be easy to determine, the malfunction of an internal mechanism (such as a
neurotransmitter problem) has not be found to be related to many instances of abnormal behaviour,
which would then mean they were not diagnosed as a mental disorder. The implications of this for
treatment are not clear.
Deviation from ideal mental health
As you will see in your text Jahoda (1958) described some characteristics that mentally healthy
people should possess. However, not everyone agrees. People from different cultures might feel
that the ideals of autonomy and independence are far from ideal and represent instead isolation.
Positive psychology and deviation from ideal mental health. Recently, a group of psychologists
including Martin Seligman (who came up with the 7 features of abnormality in 1989 with David
Rosenhan) have developed a discipline within psychology called “positive psychology”, looking at
how , why and under what conditions positive emotions and character traits flourish, and prevent
mental health problems. (See Seligman and Csikszentmihalyi, 2000, and Peterson and Seligman,
2004). They asked the question “Can psychologists take what they have learned about the science
and practice of treating mental illness and use it to create a practice of making people lastingly
happier?” (Seligman et al., 2005).
They argue that their classification of character strengths and virtues is a positive complement to the
various editions of the Diagnostic and Statistical Manual of Mental Disorders. Their list (see below)
is much more extensive than Jahoda’s and has empirical cross-cultural support (see Seligman et al.,
2005) but nonetheless could be open to debate. For example, some might argue that many of the
character strengths are dependent on good physical health and a certain amount of control over
one’s own life.
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As mentioned above, manuals of diagnostic criteria have been developed to try and help mental
health professionals distinguish between normality and abnormality. The four that you will need to
know something about are:
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Name
Diagnostic and
Statistical Manual of
Mental Disorders
(DSM)
Date of most recent edition
th
May, 2013, 5 edition ( DSM 5)
International
Classification of
Diseases (ICD)
Chinese Classification
of mental Disorders
2010, 10 edition (ICD-10)
2001, 3 edition (CCMD 3)
Chinese
Society of
Psychiatry
Great Ormond Street
criteria
Continually updated online at
http://www.gosh.nhs.uk/medicalconditions/
Great
Ormond St
children’s
hospital in
London, UK
th
rd
Published by
American
Psychiatric
Association
World Health
organization
Comments
Used in the USA,
South America
and parts of Africa
and Asia. Recent
update has
caused
controversies,
which will be
discussed as we
come to them.
Used in Europe.
th
11 edition is now
being developed.
Used in China.
Written in Chinese
and English and
has about 40
culturally related
diagnoses.
Developed
specially for
children. See
Nicholls et al.
(2000) on a
comparison of the
reliability of the
DSM, ICD and
GOS criteria when
diagnosing
childhood eating
disorders.
The development and use of these manuals is relevant in the next section of this e-text.
A study showing the difficulty of deciding what is normal or abnormal with regard to behaviour.
Todd Elder (2010) found that children who were the youngest in their class were 60% more likely
than older children to be diagnosed with attention deficit hyperactivity disorder (ADHD). In fifth
and eighth grade (when students are typically 10-11 or 13-14 years old) , the youngest students in
a class were more than twice as likely to use Ritalin, a stimulant commonly prescribed for ADHD,
compared with the oldest students. He suggests that paediatricians — who actually make the
diagnoses and prescribe treatments — should evaluate children based on their age, not their
grade.
Elder does not investigate why younger children are diagnosed with ADHD more frequently, but
newspaper reports of his study pointed out that nearly one million children in the USA may have
been misdiagnosed with this disorder (http://usatoday30.usatoday.com/news/health/2010-08-171Aadhd17 ST N.htm )
Principle that this study could be used to demonstrate
Cognitive processes are influenced by social and cultural factors.
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B. Validity and reliability of diagnosis
Learning outcome:
Discuss validity and reliability of diagnosis.
Validity and reliability of diagnosis is closely related to having an
understanding of what is normal or abnormal behaviour, and to the use
of the classificatory systems. A diagnosis is usually required before
anyone can be treated, and therefore it is important to get it right.
Validity. A valid diagnosis is when a diagnosed person really has a
particular order as defined by the diagnostic classification systems. The
problem is that it is difficult to establish this without using a system, and the systems all vary to a
lesser or greater extent. A term like major depressive disorder refers to a collection of symptoms
that vary between the three main manuals. Moreover, there are no biological diagnostic tests for
many disorders, so how can there be validity?
There is an increasing awareness that life events have a role to play in a disorder like depression,
which can be a perfectly normal response to bereavement and trauma. In the DSM IV-text revised
edition (DSM IV-TR 2000), depression after the loss of a loved one was only diagnosed as major
depressive disorder if it had continued for longer than two months. In the new DSM 5 the reference
to bereavement has been withdrawn, with the result, according to critics, that grief and anxiety will
become seen as mental illnesses. (See, for example http://www.bbc.co.uk/news/health-20986796 ).
Revision of the classifications implies revision of the symptoms and changing the validity of past
diagnoses.
Rosenhan’s famous 1973 study, described in your text, was designed to show up the inhuman
treatment suffered by psychiatric inpatients. In this interview he says that while the mental health
nurses were doing the best that they could, they needed to be reminded that patients are not just a
“collection of symptoms” but are real people with spouses, mortgages, families and friends. His
study also highlights the problem of validity of diagnosis, which in this case was non-existent. The
symptoms the pseudo-patients described (hearing voices saying “thud”, “empty” and “hollow”) are
not part of the criteria for schizophrenia in any of the manuals, and those admitted as suffering from
this disorder were not suffering from anything except a misdiagnosis.
Face validity
Face validity is when criteria appear to measure what they say they do. ADHD as an abnormal
behaviour has good face validity, in that the criteria describe the behaviour involved in what is
accepted cross-culturally by clinicians as ADHD (Canino and Alegria, 2008). However, the problem
with criteria with clear face validity is that they are more vulnerable to a social desirability bias.
Individuals may manipulate their response to deny or hide problems, or exaggerate behaviours in
order to fall within the criteria.
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Construct validity
Construct validity is to do with whether the diagnostic test administered can be used to support the
diagnosis. Can psychologists be sure that the questions asked are valid for the disorder being
tested? The only way to do this is to test the questionnaires with patients who have already been
diagnosed using other measures, and look for consistency. The psychologist Aaron Beck did this
with his Beck’s Depression Inventory, version 2, using 210 psychiatric outpatients, and found a high
level of agreement with other scales. The criteria he used were a mixture of those found in the OCD
and DSM manuals, plus agitation, concentration difficulty, worthlessness and loss of energy (Beck,
1997). He found that the questions used had high construct validity, in that those already diagnosed
through other measures as having depression, also fit the criteria with their answers to his inventory.
A study illustrating the problem of construct validity when diagnosing an eating disorder
Kelly et al. (2012) conducted research into the construct validity of several different psychometric
measures of eating disorders. The researchers expressed concern that the existing measures do
not adequately assess eating concerns among black women. They point out that most measures
of eating disorder symptoms and risk factors were developed in predominantly white female
samples. Yet eating disorders affect individuals of all racial and ethnic backgrounds. Black women
appear more vulnerable to certain forms of eating pathology, such as binge eating, and less
susceptible to other eating disorder symptoms and risk factors, such as body dissatisfaction,
compared with their white peers.
Their results suggest that scores on the eating disorders scales are not equivalent across
ethnicities. Thus, it is recommended that researchers and clinicians obtain additional information
regarding racial/cultural factors when using these instruments with black women.
Principle that this study could be used to demonstrate
Culture (social norms and values) influences behaviour.
Reliability
Reliability is basically accuracy. The two most important forms of reliability when it comes to
diagnosis are inter-rater reliability and test-retest reliability.
Inter-rater reliability
This is when another mental health professional, preferably without knowing the original diagnosis,
and using the same diagnostic system, comes to the same conclusion about a patient. Inter-rater
reliability from one psychologist to the next can be low because disorders overlap. For example,
depression and anxiety disorders have many of the same symptoms.
Pies (2007) points out the inter-rater reliability for many mental disorders is good. In fact, he points
out that it is as good as or better than the reliability for many physical disorders, including cancer
diagnoses. He argues that total objectivity is impossible, any medical field and while high interrater reliability is the goal, it is inaccurate to single out the mental health practitioners as any worse
in this respect than physicians.
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Test-retest reliability
This is the reliability of diagnosis over time. Disregarding those re-diagnoses that are due to
changing classifications, a patient who is diagnosed by a psychiatrist with a certain disorder should,
if s/he has not recovered, be diagnosed with the same disorder by the same clinician at any future
date. The diagnosis should not change. See the study by Seeman in your text.
Just a thought - if the mental health staff in Rosenhan’s study had reinterviewed the participants
immediately after their admission, they should have discharged all of them. If they were admitted
because they heard voices, then hearing no voices would logically be sufficient for discharge.
However, as Rosenhan points out, diagnostic labels are “sticky” and all subsequent behaviour
becomes interpreted in the light of the original diagnosis (1973, p 257). This is probably relevant for
test-retest reliability; why would a clinician change his or her original diagnosis?
C. Cultural and ethical considerations in diagnosis
Learning outcome:
Discuss cultural and ethical considerations in diagnosis
Diagnosis is the identification of groups or patterns of mental
symptoms that reliably occur together to form a type of disorder. Just
as reliability and validity are related to beliefs about what is normal
and abnormal, so are cultural and ethical considerations relevant
when looking at validity of diagnosis. Constructs (definitions) used for
majority populations may not be valid for minorities, and psychologists
are subject to biases when interviewing people from lower socioeconomic groups, from unfamiliar cultures or who cannot articulate
their problems adequately.
1. Cultural considerations
Different cultures have different criteria for judging what is normal and abnormal, and different ways
of explaining abnormal behaviour. For example, the main problems with cross-cultural diagnosis
are: culture-bound syndromes that do not exist outside of their own society; mental health
professionals’ culture blindness and cultural stereotypes; reporting bias and symptoms vary crossculturally.
Culture-bound syndromes
If a particular abnormal behaviour or mental disorder does not exist outside the culture of a patient,
and they come to a psychiatrist or psychologist who is not from their culture, then the clinician will
not have the tools with which to diagnose and will be as puzzled as anyone else, unless they has
taken care to inform themselves about mental disorders from different cultures. This may well result
in a misdiagnosis and mistreatment. Two examples of culture bound syndromes are:
•
•
amok or mata elap: (Malaysia) which is characterized by a period of brooding followed by an
outburst of violent, aggressive, or homicidal behaviour directed at people and objects. The episode
tends to be precipitated by a perceived insult and seems to be prevalent only among males. It is
sometimes the first symptom of a serious mental disorder.
shenjian shuairuo: (Chinese) equivalent to a diagnosis of "neurasthenia". Symptoms include
physical and mental fatigue, dizziness, headaches and other pains, difficulty concentrating, sleep
disturbance, and memory loss. Other symptoms include gastrointestinal problems, sexual
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dysfunction, irritability, excitability, and various signs suggesting disturbances of the autonomic
nervous system. Very similar to the Western diagnosis of major depressive disorder, but often
without the lowered mood.
See here for the website of a psychologist and psychiatrist with a special interest in culture-bound
syndromes.
The American Psychiatric Association has not included a comprehensive list of culture-bound
syndromes in the DSM-5, though some cultural syndromes are detailed in the Appendix of the
manual. Instead, the criteria for each disorder have been updated where relevant to reflect crosscultural variations in presentations, and to give more detailed and structured information about
cultural concepts of distress. They explain with two examples:
1. Uncontrollable crying and headaches are symptoms of panic attacks in some cultures, while
difficulty breathing may be the primary symptom in other cultures.
2. The criteria for social anxiety disorder now include the fear of “offending others” to reflect the
Japanese concept in which avoiding harm to others is emphasized rather than harm to oneself.
(APA, 2013)
While this widens the criteria and makes them more sensitive, it does not solve the problem of totally
different disorders being present in some cultures.
An important thing to note is that all disorders are culture-bound, including all Western disorders, as
they arise in a cultural context. No psychological disorder can escape a cultural influence (see
Marsella, 2010 for further discussion of this).
Culture blindness and cultural stereotypes
As was outlined earlier, there are cross-cultural differences in what is perceived as abnormal
behaviour. It is not uncommon for example, in some cultures, to see or hear deceased relatives. So,
this should not always be considered as a symptom of a psychological disorder. Studies in New
Zealand show that the Maori and Pacific islanders have different definitions from the New
Zealanders from a European background for what is and is not a mental health issue. Using the
DSM IV, affective disorders account for only 16% of diagnoses given to Maori mental health patients
(compared with 30% for Europeans), whereas 60% of diagnoses of Maoris were for schizophrenia,
compared with 40% for Europeans (Tapsell and Mellsop, 2007 in Law et al., 2010). The symptoms
presented by Maoris are normal in their culture – seeing or hearing the deceased, mental withdrawal
when feeling at a disadvantage – but can be interpreted as symptoms of schizophrenia by
psychiatrists with a lack of cultural understanding.
Interpretation of another’s culture is always difficult, and if not careful, it is very easy to revert to
cultural stereotypes. Once this happens, then the evidence can seem to reinforce this. Cultural
stereotyping can occasionally have severe health consequences. Andary et al. describe the case of
a “Mediterranean man” (their term) who while hospitalised in a psychiatric inpatient unit complained
of severe headaches. As he frequently tended to complain of various vague medical symptoms,
staff dismissed his complaints as signs of his “Mediterranean temperament”. Shortly after this he
suffered a stroke (2003, p 96).
Singh et al. (2007) documented that in the UK, black patients were 3.83 times and Asian patients
2.06 times more likely to be detained under the 1983 Mental Health Act. This would suggest to the
less well-informed that people from these groups have more incidences of mental illness that cannot
be controlled outside of the residential setting, and thus cultural blindness in treating different
symptoms as more serious, leads to cultural stereotyping of people from ethnic minorities as more
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seriously affected by mental disorders.. However, Singh et al. point out that the picture is much
more complex than this. They also dismiss explanations of pure racism, and argue for the central
collection of data relating to both assessment and detention so that further comparisons may be
made.
A study illustrating the problem of cultural stereotypes when diagnosing
Burr (2002) investigated how cultural stereotypes of women from South Asian communities
affected mental health care professionals' explanations for patterns of suicide and depression.
Low rates of treated depression and high rates of suicide in women from some South Asian
communities are evident in data from the UK. Burr argued that explanations for these apparent
differences are likely to be located in stereotypes of “repressive” South Asian cultures. This
qualitative piece of research, using focus groups and individual interviews, sought to explore the
construction of cultural stereotypes within mental health discussion with specific reference to
stereotypes of women from South Asian communities.
Mental health carers from a UK inner city area of relatively high social deprivation were targeted.
Focus group interviews were conducted with a range of mental health care professionals who
worked in both inpatient and outpatient mental health care services. In addition, individual
interviews were conducted with consultant psychiatrists and general medical doctors.
Analysis of data from the interviews suggests how health carer's knowledge about and experience
of South Asian cultures led to them constructing cultural difference in terms of unchanging
categories constructed upon stereotypes of western culture as superior to a construction of
eastern cultures as repressive, patriarchal and inferior to a western cultural ideal. Ultimately, Burr
argues, these stereotypes become incorporated as 'fact' and have the potential to misdirect
diagnosis (leading to under-estimation of depression) and therefore, also miss opportunities to
treat appropriately.
Principles that this study could be used to demonstrate
Cognitive processes are influenced by social and cultural factors.
Culture (social norms and values) influences behaviour.
(Note that one of these is from the CLOA and one from the SCLOA)
Reporting bias
Reporting bias occurs because data is gathered concerning those who
have been identified as having a particular disorder. If they are not
diagnosed, because their symptoms are not recognised as such or
because they do not go to the doctor; or if they are misdiagnosed, then
they do not show in the statistics.
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Angel and Thoits (1987) show how cognitive interpretations of symptoms vary between different
cultures, and affect the reporting and subsequent diagnosis of mental disorders. The example they
give is of the underreporting in Mexico of certain mental disorders. They describe three stages of
illness definition: pre-symptom (when emotional changes are noticed), labelling and course of
action. It is at these last two stages that reporting bias can be observed. The symptoms are
compared to those of the home culture, and if they seem to be symptoms of something that is
stigmatised (viewed negatively in the person’s culture) then they are less likely to be reported to a
medical professional, and traditional medicine or folk cures are more likely to be sought.
Sato (2006, in Law et al. 2010) discusses how schizophrenia has been renamed in Japan because
there was such a stigma attached to it that less than 40% of patients diagnosed with it had been told
of their diagnosis. These patients would show in the statistics for this mental disorder, but there is a
high chance that the stigma associated prevents others with possible symptoms from seeking
medical help.
Cross-cultural variations in symptoms
Some of this has been touched on above. The symptoms of the mental disorders in the two main
manuals (DSM 5 and ICD-10) are not necessarily the symptoms that will be present in patients from
some ethnic minority groups. The researchers of the DSM 5 have tried to remedy this (see earlier),
and when the ICD-11 is published in 2014, maybe this will also be addressed there.
Examples given in your text are that people from East Asia (especially China) will exhibit more
somatic (physical) symptoms when depressed than their western counterparts and another example
is that black patients in the UK with bipolar disorder (called manic depression in the UK) report fewer
suicidal thoughts and more manic episodes, which leads them to sometimes be diagnosed with
schizophrenia instead (Kirov and Murray, 1999). See this link to an article by Ethan Watters in the
New York Times, on both cross-cultural and historical variations in symptoms and what is classified
as a mental disorder.
A study illustrating the issue of differing symptoms across cultures.
Stewart et al. (2004) gathered information about their diagnosed depression from adolescents
(N=2,272) in Hong Kong and the United States. The adolescents provided information regarding
their depressive symptoms, cognitions (*self-efficacy, negative beliefs, and hopelessness), and
stressful events in 2 surveys conducted 6 months apart. Depressive symptoms and hopelessness
were higher and self-efficacy and negative beliefs were lower, in Hong Kong than in the United
States. There was some support for the hypothesis that self-efficacy is a less relevant descriptor in
collective compared with individualistic cultures. These findings show how symptoms can vary
from culture to culture, though notably in this case this had not resulted in differing diagnoses.
*self-efficacy = one’s belief in one’s ability to succeed.
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2. Ethical considerations
As can be seen in the previous examples and discussion, there is a large overlap between cultural
and ethical considerations in diagnosis. Those not diagnosed, misdiagnosed or mistreated because
of their culture are already being treated unethically. Central issues in the ethics of diagnosis are
stigmatization, self-fulfilling prophecy and confirmation bias.
Stigmatization
The word stigma is defined as “the shame or disgrace attached to something regarded as socially
unacceptable” (Encarta online dictionary, 2009). Therefore stigmatization of those with a mental
disorder is treating them as if they should be ashamed, as if they are in disgrace, because to have a
mental disorder is socially unacceptable. Before we say to ourselves that we would never do that,
think about if your teacher revealed that they had previously been hospitalized for depression, or
your sports coach said that they function much better when on their medication for their bipolar
disorder. The very fact that this information is much less likely to be revealed than that concerning a
physical problem already shows that there is a stigma attached to it. After all, your reaction if your
teacher mentions, “Oh, yes, I broke my collar bone last year,” is likely to be much less strong than
your reaction to their previous depression.
Goffman (1968) wrote about the stigmatizing consequences for the individual of labelling a particular
action or pathological state as deviant, and Rosenhan’s (1973) study shows how once labelled, a
person’s actions are all framed within that label.
More recently, researchers have described the experience of stigmatization at the level of the
individual, and differentiated between: self-imposed stigma due to shame, guilt and low self-esteem;
socially imposed stigma due to social stereotyping and prejudice; and structurally imposed stigma,
caused by policies, practices, and laws that discriminate against the mentally ill (see ArboledaFlorez and Sartorius, 2008, for example).
A very worrying article published recently in the New York Times newspaper draws attention to what
is called “diagnostic overshadowing”, which is when a doctor gives different treatment for their
physical illness to someone suffering from a mental disorder, because their mental health diagnosis
“overshadows” their identity as a person who needs some physical treatment (Garey, 2013). The
links in this article provide plenty of evidence of discrimination. Stigmatization of those with mental
disorders does not seem to be decreasing over the years
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A study into stigmatization of moderate to severe depression
Schwenk et al. (2010) investigated the concerning prevalence of depression and suicidal thoughts
among medical students, a group that may experience poor mental health care due to
stigmatization. The study was conducted in 2009, covering all students enrolled at the University
Of Michigan Medical School. A little more than 65% participated in the survey—505 students out of
769 enrolled.Their aim was to examine the perceptions of depressed and non-depressed medical
students regarding the stigma associated with depression.
Outcomes of the study revealed that 14.3% of the students were identified as having moderate to
severe depression, higher than the 10-12% range found in the population at large. The results also
revealed that 53.3% of medical students who reported high levels of depressive symptoms were
worried that revealing their illness would be risky. Almost 62% of the same students said asking for
help would mean their coping skills were inadequate.
The researchers suggested that new approaches may be needed to reduce the stigma of
depression and to enhance its prevention, detection, and treatment. “The effective care of mental
illness, the maintenance of mental health and effective emotional function, and the care of
professional colleagues with mental illness could be taught as part of the ethical and professional
responsibilities of the outstanding physician and become a critical component of the teaching, role
modelling, and professional guidance that medical students receive as part of their curriculum in
professionalism.”
Principles that this study could be used to demonstrate
Human beings are social animals with a basic need to “belong”.
People’s views of the world are resistant to change.
Self-fulfilling prophecy
A self-fulfilling prophecy is the process by which expectations of other people or groups lead those
persons or groups to behave in ways that confirm those expectations. The term “self-fulfilling
prophecy” was first used in 1948 by Robert K. Merton, who drew upon W. I. Thomas's statement: “if
men define situations as real, they are real in their consequences.” (See an excellent review by
Wineberg, 1987). It is a term that you should be familiar with through Rosenthal and Jacobson’s
(1968) study Pygmalion in the Classroom. (See your text, p 18 to remind yourself).
This again is related to labelling. When we are labelled as something, the self-fulfilling prophecy
theory would argue that we internalise this label and our belief that we are really “depressed”,
“manic”, or even just “different” means that we act in a way that makes this label, and the attached
prediction about our behaviour, come true. In other words, the belief makes reality conform to the
belief. While me may not become depressed merely by being labelled depressed, knowing that we
are depressed may make us isolate ourselves and feel powerless to change our situation.
Self-fulfilling prophecy may also relate to difficulties in functioning in life. A person with a disorder
who takes time off work can find it difficult to return and end up losing their job and becoming more
isolated and depressed. See this interesting blog post about the difference between “being” bipolar
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and “having” bipolar disorder. Being labelled as “having” a disorder allows people with the disorder
to resist the power of self-fulfilling prophecy.
Confirmation bias
Confirmation bias is a tendency to search for or interpret information in a way that confirms one's
preconceptions. In the area of abnormal psychology, confirmation bias is when psychologists and
psychiatrists interpret behaviour as fitting in with their original diagnosis of the disorder, and ignore
any behaviour that does not. Rosenhan (1973) points out that the note-taking by the pseudo patients
was written up in their medical notes as “writing behaviour”, and nobody ever showed any curiosity
as to what they were writing.
More recent research supports the theory. Parmley found confirmation bias to be “powerful and
ubiquitous” and recommends more studies be done into finding a remedy (2006, p 116).
A study into confirmation bias
Mendel et al. (2011) researched the existence of possible confirmation bias in mental health
professionals. To study whether psychiatrists and medical students are prone to confirmation bias
and whether confirmation bias leads to poor diagnostic accuracy in psychiatry, they presented an
experimental decision task to 75 psychiatrists and 75 medical students.
They found that 13% of psychiatrists and 25% of medical students showed confirmation bias when
searching for new information after having made a preliminary diagnosis. Moreover, psychiatrists
conducting a confirmatory search for information that supported their diagnosis made a wrong
diagnosis in 70% of the cases compared to 27% or 47% for a contradictory information or
balanced information search. Participants choosing the wrong diagnosis also prescribed different
treatment options compared with participants choosing the correct diagnosis.
The researchers’ conclusion was that confirmatory information search carries with it the risk of
wrong diagnostic decisions. Psychiatrists should be aware of confirmation bias and instructed in
techniques to reduce bias.
Principle that this research method example could be used to demonstrate
People’s views of the world are resistant to change.
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3. Psychological disorders
A. Symptoms and prevalence
Learning outcome:
Describe symptoms and prevalence of one disorder from two of the following groups.
Discuss cultural and gender variations in prevalence of disorders.he world are resistant to change.
i.
ii.
iii.
Affective disorders (major depressive disorder)
Anxiety disorders (post-traumatic stress disorder)
Eating disorders (bulimia nervosa)
A symptom is any feature of a physical or mental disorder noticed by the patient. Prevalence is the
total number of cases of a disease in a given population at a specific time. Lifetime prevalence is the
percentage of people who have had the diagnosis at some point in their life. (Encarta online
dictionary, 2009)
i.
Affective disorders (major depressive disorder)
Symptoms. Affective disorders are disorders related to mood. For the
purposes of the IB Diploma, in this section we will be examining major
depressive disorder (MDD).
The DSM -5 (below) did not change the criteria for categorizing the
symptoms of MDD from those in the DSM-IV, except to controversially
remove the requirement given later in the DSM IV that these symptoms
are not occurring within two months after bereavement, such as the
loss of a loved one. See a recent BBC news article that argues for
reinstating the “bereavement exclusion” and this easy to read response to critics of this change in
the DSM 5. There is a link made in this article that might be useful in TOK. It concerns the thinking
behind psychology and takes us back to the normal/abnormal debate, this time over how long it is
normal to grieve.
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DSM-5 Criteria for Major Depressive Disorder (MDD)
• Depressed mood or a loss of interest or pleasure in daily activities for more than two weeks.
• Mood represents a change from the person's baseline.
• Impaired function: social, occupational, educational.
• Specific symptoms, at least 5 of these 9, present nearly every day:
1. Depressed mood or irritable most of the day, nearly every day, as indicated by either subjective
report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful).
2. Decreased interest or pleasure in most activities, most of each day
3. Significant weight change (5%) or change in appetite
4. Change in sleep: Insomnia or hypersomnia
5. Change in activity: Psychomotor agitation or retardation
6. Fatigue or loss of energy
7. Guilt/worthlessness: Feelings of worthlessness or excessive or inappropriate guilt
8. Concentration: diminished ability to think or concentrate, or more indecisiveness
9. Suicidality: Thoughts of death or suicide, or has suicide plan
(DSM 5, 2013)
Prevalence
It is very difficult to place a figure on the percentage of the world’s population that are suffering at
any one time from MDD. The Global Burden of Disease (GBD) 2010 Study tried to do this with many
physical and mental disorders. Below is an explanation of how the data for the report was gathered.
Gender. To summarise, the figures in the Global Burden of Disease (2010) study gave the
prevalence of MDD worldwide as 4.4%, with 298 million cases globally, with women more likely to
be represented than men. Explanations for more women than men being diagnosed with MDD are
covered in your textbook, and range from biological (hormones and genes), cognitive (women are
more prone to lowered mood and guilt) and sociocultural (women are more likely to go to the doctor
when they feel depressed, and male doctors, having stereotypical beliefs about women, are more
likely to diagnose them as depressed; women are more isolated than men, often being at home with
children). More research from both an emic and etic approach is needed.
Culture. All of the cultural considerations that have already been discussed must be taken into
account when evaluating prevalence data on MDD. (Culture blindness, reporting bias, cross-cultural
variation in symptoms, etc.) The National Institute for Mental Health puts the prevalence of MDD in
the States at 6.7% and any internet search will come up with varying statistics for different regions of
the world.
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Study showing how the prevalence rates for MDD were collated, for the GBD 2010 study
Ferrari et al. (2013) conducted a study of the literature in order to present a global summary of the
prevalence and incidence of MDD, accounting for sources of bias, and dealing with heterogeneity.
The researchers noted that summarizing the epidemiology of major depressive disorder (MDD) at
a global level is complicated by significant differences in the data.
They undertook a systematic review of prevalence and incidence of MDD, searching electronic
databases Medline, PsycINFO and EMBASE. Community-representative studies were included.
The results suggested that there were over 298 million cases of MDD globally at any point in time
in 2010, with the highest proportion of cases occurring between 25 and 34 years. Prevalence was
very similar across time (4.4% in 1990, 4.4% in 2005 and 2010), but higher in females (5.5%)
compared to males (3.2%) in 2010.
Regions in conflict had higher prevalence than those with no conflict. The annual incidence of an
episode of MDD followed a similar age and regional pattern to prevalence but was about one and
a half times higher, consistent with an average duration of 37.7 weeks.
Good-quality estimates from low-/middle-income countries were sparse. More accurate data on
incidence are also required
Principle that this study could be used to demonstrate
Culture (social norms and values) influences behaviour.
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ii.
Anxiety disorders (post-traumatic stress disorder)
Symptoms
With PTSD the body's response to a stressful event is changed.
Normally, after the event the body recovers. The stress hormones and
chemicals the body releases due to the stress go back to normal levels.
For some reason in a person with PTSD the body keeps releasing the
stress hormones and chemicals.
Most texts on PTSD are agreed three kinds of symptoms that the
psychologist looks for: re-experiencing symptoms, avoidant symptoms
and symptoms of increased arousal. In order to be defined as
symptoms, these have to last for 30 days or more.
1. Reliving the event, which disturbs day-to-day activity – flashbacks, memories, nightmares,
strong reactions to situations that remind the person of the event, feeling guilty about the event.
2. Avoidance- emotional numbing, feeling detached, memory gaps of the event, avoiding places
and people that remind the person of the event, feeling hopeless.
3. Hyperarousal – always scanning surroundings for signs of danger, unable to concentrate, startle
easily, outbursts of anger, sleep problems.
See here for the DSM 5 criteria for PTSD. Note that the DSM 5 contains one set of criteria for those
over 6 years old, and another set for those of 6 years and under.
However, there is definite evidence of cross-cultural differences in symptoms. Watters (2010) writes
this, about PTSD in the wake of the Asian tsunami of December 2004, “After the 2004 tsunami in
Asia, many mental-health experts agreed that a ‘second tsunami’ of mental illness in the form of
PTSD would strike the region. …. A few years on, however, their efforts [to help] have raised a
troublesome question: were they bringing the wrong treatment to the wrong people?” At issue is
not whether tragic events like the tsunami trigger debilitating psychological distress and even mental
illness, but over the extent to which survivors’ cultural beliefs shape their symptoms. If culture has
the impact that some researchers suggest, the PTSD diagnosis may be of little help (and even do
potential harm) when applied wholesale in other countries.
Allan Young, a medical anthropologist at McGill University in Montreal, states that while reactions to
trauma vary across cultures, they also vary across time, using the example that soldiers who fought
in wars in different decades experienced different outward symptoms as a function of the societal
views of their time. He notes that although symptoms vary across time and culture, it is important to
recognize that they are always very real to the person experiencing them (2004, pp 127-146).
Prevalence
Marsella (2010) points out that in spite of what appears to be common neurological processes, in
the initial response to a traumatic event, cultural variables exercise a major influence on perceived
causes, symptoms and responses of society to PTSD. Determining global prevalence therefore
suffers from the same difficulties as with major depressive disorder.
Gender. The National Comorbidity Survey Replication (NCS-R), conducted between February 2001
and April 2003 in the USA comprised interviews of a nationally representative sample of 9,282
people aged 18 years and older. PTSD was assessed among 5,692 participants, using DSM-IV
criteria. The NCS-R estimated the lifetime prevalence of PTSD among adult Americans to be 6.8%.
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Current past year PTSD prevalence was estimated at 3.5%. The lifetime prevalence of PTSD
among men was 3.6% and among women was 9.7%. The twelve month prevalence was 1.8%
among men and 5.2% among women (Kessler et al, 2005). Again, reasons for women suffering
more PTSD are given in your textbook. The most commonly-cited reason is that women are more
likely than men to experience sexual assault of one kind or another, and this is a likely cause of
PTSD.
The 2010 Australian Bureau of Statistics figures on mental illness indicate that 6.3% of all
Australians suffer from PTSD – 50% more than suffer from the well-known effects of depression. A
recent Australian report into homeless men living on the streets gave their rates of PTSD as 20%
(MISHA, 2012).
Culture. In a previous WHO World Mental Health survey of 21 countries, more than 10% of
respondents reported witnessing violence (21.8%) or experiencing interpersonal violence (18.8%),
accidents (17.7%), exposure to war (16.2%) or trauma to a loved one (12.5%). The survey indicated
that an estimated 3.6% of the world's population has suffered from post-traumatic stress disorder
(PTSD) in the previous year.
However, responses to trauma vary culturally, as do symptoms of PTSD. Watters (2010) discusses
cultural differences in reaction to trauma. He uses events following the 2004 tsunami as example,
describing how western therapists arrived in Sri Lanka to provide counselling and treatment for
PTSD without really considering the effect culture has on outward symptoms and coping
mechanisms resulting from exposure to a traumatic event. Using a North American designed and
tested PTSD checklist of symptoms, the volunteer trauma counsellors diagnosed 14% to 39% of
children with PTSD within 3 to 4 weeks of the tsunami. This is despite the fact that the DSM-IV
diagnostic criteria requires that symptoms cause significant distress or impairment in functioning for
over a month before one can be given the diagnosis.
Immediately following the tsunami, Sri Lankan peoples’ top priority seemed to be aiding those
around them, rather than seeking treatment themselves, behaviours that were viewed by many of
the therapists as signs of “denial” and “shock,” and considered to be warning signs of
PTSD. Despite the persistence of Sri Lankans to continue helping those around them, the
therapists continued encouraging them to stop and “take care of themselves first.” However, in
many cultures, the practice is to help others before you help yourself.
No culture is immune to the pain and suffering caused by catastrophic or life-threatening events, but
there are important cultural differences in how these events are interpreted and dealt with. Therefore
best diagnostic practices (on which prevalence rates are built) in one culture cannot necessarily be
applied to another.
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Study into the prevalence of PTSD in adolescents
McLaughlin et al (2013) conducted a large-scale study into traumatic experience and PTSD in
adolescents, using a sample of over 6,000 adolescent and parent pairs in a national survey of
adolescents aged 13-17 years. Although exposure to traumatic experiences is common among
youths in the United States, information on PTSD risk associated with this is limited. The
researchers found that a majority (61.8%) of adolescents experienced a traumatic event in their
lifetime, and lifetime prevalence of PTSD according to the DSM-IV criteria was 4.7% and was
significantly higher among females (7.3%) than among males (2.2%).
Exposure to traumatic experiences, particularly interpersonal violence, was highest among
adolescents not living with both biological parents and having pre-existing behaviour disorders.
Conditional probability of PTSD was highest for PTEs involving interpersonal violence. Predictors
of PTSD among PTE-exposed adolescents included female gender, prior PTE* exposure, and preexisting fear and distress disorders. One-third (33.0%) of adolescents with lifetime PTSD
continued to meet the criteria within 30 days of interview, with poverty, having bipolar disorder, and
suffering a second traumatic experience all being predictors of non-recovery.
The researchers concluded that interventions designed to prevent PTSD in trauma-exposed
youths should be targeted at victims of interpersonal violence with pre-existing mental disorders,
whereas interventions designed to reduce ongoing PTSD should attempt to prevent exposure to a
second traumatic experience.
*PTE = Previous Traumatic Event.
iii Eating disorders (bulimia)
Symptoms
Bulimia nervosa is characterized by frequent episodes of binge eating followed by inappropriate
behaviours such as self-induced vomiting to avoid weight gain. DSM-5 criteria reduce the frequency
of binge eating and compensatory behaviours that people with bulimia nervosa must exhibit, to once
a week from twice weekly as specified in DSM-IV.
Lewinsohn et al. (2002) noted in their study into gender differences in eating
disorder symptoms in young adults that women scored much higher on body
dissatisfaction than men, and indeed fitted more of the criteria, except for
excessive exercise, with men engaging in significantly more excessive
exercise after bingeing.
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According to the DSM-5 criteria, ABNORMAL
to be diagnosed
as having bulimia nervosa a person must
PSYCHOLOGY
display:
•
Recurrent episodes of binge eating. An episode of binge eating is characterised by both of
the following:
•
Eating, in a discrete period of time (e.g. within any 2-hour period), an amount of food that
is definitely larger than most people would eat during a similar period of time and under
similar circumstances.
•
A sense of lack of control over eating during the episode (e.g. a feeling that one cannot
stop eating or control what or how much one is eating).
•
Recurrent inappropriate compensatory behaviour in order to prevent weight gain, such as
self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting, or
excessive exercise.
The binge eating and inappropriate compensatory behaviours both occur, on average, at least
*once a week for three months. (Eating Disorders Victoria website, 2013)
*(this is a change from DSM-IV, which stated twice a week).
Prevalence
Because doctors are not required to report eating disorders to a health agency, and because people
with these problems tend to be secretive, denying that they even have a disorder, we have no way
of knowing exactly how many people are affected.
We can study small groups of people, determine how many of them are eating disordered, and then
extrapolate to the general population. The numbers are usually given as percentages, and they are
as close as we can get to an accurate estimate of the total number of people affected by eating
disorders. Large scale studies have also been conducted, relying on standardised measurement
scales, interviews and self-reporting.
Gender. Prevalence rates in Western countries for anorexia nervosa ranged from 0.1% to 5.7% in
female subjects. Prevalence rates for bulimia nervosa ranged from 0% to 2.1% in males and from
0.3% to 7.3% in female subjects in Western countries. Prevalence rates in non-Western countries
for bulimia nervosa ranged from 0.46% to 3.2% in female subjects. Studies of eating attitudes
indicate abnormal eating attitudes in non-Western countries have been gradually increasing (Makino
et al., 2004)
Culture. With the exceptions of Japan and a recent study in Iran, prevalence estimates of bulimia in
non-Western nations were below the range reported for Western nations in the DSM–IV–TR. They
concluded that the degree of Western influence may account for a good deal of variance in bulimia
prevalence estimates.
Makino et al. (2004) report that prevalence rates for bulimia nervosa range from 0% to 2.1% in
males and from 0.3% to 7.3% in female subjects in Western countries. Prevalence rates in nonWestern countries for bulimia nervosa range from 0.46% to 3.2% in female subjects, with no data for
males. Studies of eating attitudes indicate that abnormal eating attitudes in non-Western countries
have been gradually increasing.
The data from both of these studies would suggest that bulimia nervosa has a sociocultural etiology
(i.e. an environmental cause) rather than a biological, though we must remember the possibility of
reporting bias and different diagnosis. The etiology of bulimia nervosa is something that will be
looked at later.
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Study into the prevalence of eating disorders, especially bulimia
In a study in the USA, Hudson et al. (2007) analysed data from 2,980 adults who were asked about
eating disorders. They found that 0.9% of women and 0.3% of men reported having anorexia
nervosa at some time in their lives, and 1.5% of women and 0.5% of men reported having bulimia
nervosa. People with bulimia had their condition for about eight years, which is longer than the 1.7
years reported for anorexia nervosa, though that may be a reflection of the fact that people with
long-term anorexia were reluctant, or unable, to participate in the study.
The study also found that people with eating disorders, regardless of the type, often have coexisting
mood, anxiety, impulse-control, or substance use disorders.
This study seems to show that approximately one third of people with these two eating disorders in
the USA are male, which is a higher proportion than the 10-15% identified by Carlat and Carmago
in 1991, in their database search of US records of people with bulimia between 1966 and 1990.
Principles that this study could be used to demonstrate
Cognitive processes are influenced by social and cultural factors.
Culture (social norms and values) influences behaviour.
(Note that one of these is from the CLOA and one from the SCLOA)
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Etiologies (biological, cognitive and sociocultural factors)
Learning outcome:
Analyse etiologies (in terms of biological, cognitive and/or sociocultural factors) of one disorder from
two of the following groups:
i.
Affective disorders (major depressive disorder)
ii.
Anxiety disorders (post-traumatic stress disorder)
iii.
Eating disorders (bulimia nervosa)
Discuss cultural and gender variations in prevalence of disorders.
i. Etiology of affective disorders (major depressive disorder)
Etiology of MDD – biological factors
Areas of interest to psychologists looking at biological influences on MDD have been genetic
influences, brain activity and biochemical imbalances.
Genetic influences
The risk of MDD rises if you have a parent or sibling with the disorder
(Sullivan et al., 2000). If one identical twin has MDD, then there is an
approximately 50% chance that at some time the other twin will also be
diagnosed with it. Kendler et al (2006) conducted a huge study in
Sweden, with personal interviews of 42,161 twins, including 15,493
complete pairs, from the national Swedish Twin Registry. The
researchers estimated the heritability of MDD at 35-40%, with
heritability being significantly higher in women than men (42% to 29%).
They found that twin pair resemblance for lifetime MDD was not
predicted by the number of years the twins had lived together in the home of origin or by the
frequency of current contact. This tends to support the idea of a biological, rather than a
sociocultural etiology.
This leads to the question as to why women should be so much more likely than men to inherit a
predisposition to MDD, which is something that is not answered in the biological research. This
gender imbalance in the incidence of MDD is something we will address when we look at
sociocultural factors in etiology.
In an effort to try and determine the genes that put people at risk of developing MDD, some
researchers have turned to linkage analysis. This involves finding families in which MDD has
appeared across several generations and then examining the DNA from affected and unaffected
family members, looking for differences (Plomin and McGuffin, 2003). If you are interested in
linkage analysis, this page gives a clear outline of how it works with regard to finding disease genes.
The study below shows how far psychologists and biologists have to go in trying to identify a role for
any particular gene in MDD.
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Study into biological factors in the etiology of MDD
Risch et al. (2009) investigated the genetic background to MDD and found that a certain gene
variation long thought to increase risk in conjunction with stressful life events actually may have no
effect. This serotonin transporter gene (5HTTLPR) was argued in a 2003 study by Caspi et al.to
increase the risk of major depression in people who had a number of stressful life events over a fiveyear period. However, attempts to replicate these findings have had inconsistent results.
To examine whether the 2003 study's finding could be confirmed, Risch et al. reviewed relevant
replication studies. The researchers did a meta-analysis, re-analysing data on 14,250 participants in
14 studies published from 2003 through March 2009. Of these, the researchers also re-analysed
original data, including unpublished information, on 10,943 participants from 10 studies published
before 2008. The data was re-analysed to see whether there were associations between the
serotonin transporter gene, stressful life events, and depression.
By applying the same methods used in the 2003 study, the researchers found a strong association
between the number of stressful life events and risk of depression across the studies. However, the
serotonin transporter gene did not show a relationship to increased risk for major depression, either
alone or in interaction with stressful life events, in the analysis of the 14 studies.
Recent research is still focusing on the 5HTTLPR gene, but looking at a diversity of its functions,
rather than just its role with regard to serotonin.
Principle that this study could be used to demonstrate
There are biological correlates to behaviour.
Etiology of MDD – cognitive factors
According to the cognitive model of the etiology of MDD, it is our
thoughts and beliefs that shape our behaviour and emotions. The
role of cognitive processing in emotion and behaviour is a main
factor in determining how we perceive, interpret, and assign
meaning to an event. (“It is not what happens to you, it is how you
feel about it.”) According to the cognitive model, psychological
distress is dependent on your personality as shaped by schemas, cognitive structure and your
assumptions, acquired through your life experience and your interpretation of that experience.
The most prominent psychologist associated with this theory is Aaron Beck, who proposed that
depression results when people's attributions for external events are based on maladaptive beliefs
and attitudes. Beck argued that "deviation from logical and realistic thinking was found at every
level of depression from mild neurotic to severe psychotic" (1967, p 240). Some typical themes are
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found in the ideas of depressed patients that differ significantly from that of non-depressed
individuals. Themes of low self-evaluation, ideas of deprivation, exaggeration of problems and
difficulties, self-criticism, self-commands, and wishes to escape or die are commonly found among
people with MDD. This “cognitive vulnerability” is a high risk factor for depression.
The cognitive model of depression assumes three specific concepts that result in cognitive
vulnerability:
a) the cognitive triad – a negative view of oneself, the world, and the future
b) schemas - patterns of maladaptive thoughts and beliefs
c) cognitive errors - faulty thinking accompanied by negative and unrealistic representations of
reality (Beck, 1967 and 1979).
a) Cognitive Triad - a pattern of reportable depressive thoughts that consist of :
•
Negative view of self (perceived as deficient, inadequate, or unworthy)
•
Negative view of the world (interactions with others and life in general are perceived as
difficult or hopeless)
•
Negative view of the future (current difficulties or suffering will continue indefinitely).
b) Schemas - maladaptive beliefs and attitudes that become active when we are under stress,
especially during bad circumstances. In other words, it is how we interpret the world around us and
how we assign positive and negative meaning to whatever happens to us.
c) Cognitive Errors – are also known as cognitive distortions. They are inaccurate thoughts are
usually used to reinforce negative thinking or emotions — telling ourselves things that sound rational
and accurate, but really only serve to keep us feeling bad about ourselves.
For instance, a person might tell themselves, “I always fail when I try to do something new; I
therefore fail at everything I try.” This is an example of “black or white” (or polarised) thinking. The
person is only seeing things in absolutes — that if they fail at one thing, they must fail at all things. If
they added, “I must be a complete loser and failure” to their thinking, that would also be an example
of overgeneralization — taking a failure at one specific task and generalizing it their very self and
identity. Grohol (2009) lists fifteen common cognitive distortions, of which polarised thinking and
overgeneralisation are just two.
_______________
A recent study by Haeffel and Hames (2013) investigated if changes in cognitive vulnerability
would occur during major life transitions, such as starting college. They tested the hypothesis that
cognitive vulnerability could change via a contagion effect. In other words, the negative cognitive
thought patterns associated with vulnerability to depression could be “caught” from one’s
roommate. They tested this hypothesis with a sample of randomly assigned college roommate pairs
(103 pairs of students new at college), and found that participants who were randomly assigned to a
roommate with high levels of cognitive vulnerability were likely to “catch” their roommate’s cognitive
style and develop higher levels of cognitive vulnerability. Moreover, those who experienced an
increase in cognitive vulnerability had significantly greater levels of depressive symptoms over the
time of the study than those who did not.
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Study into cognitive factors in the etiology of MDD
Beshai et al. (2012) conducted a cross-cultural study of depressed individuals in Canada (186
participants) and Egypt (150 participants) to test Beck's (1979) cognitive triad theory, which states
that depressed individuals hold negative, automatic thoughts about the self, the world and the
future. Despite the central role of Beck’s theory of the cognitive triad, it has rarely been tested crossculturally.
This study examined the relationship between feeling unhappy over a long term and a number of
inventories designed to assess negative cognitions. Unhappy and anxious individuals in both
countries harboured significantly more negative thoughts toward self, world and future than a control
group. Additionally, Egyptian participants showed significantly more negative thoughts toward self
and world than their Canadian counterparts even after controlling for feelings of unhappiness. This
research supports the cross-cultural validity of the cognitive theory for MDD.
Principle that this study could be used to demonstrate
Cognitive processes are influenced by social and cultural factors.
To summarise, cognitive theories assume that people's attributions for events, their perceptions of
control and self-efficacy, and their beliefs about themselves and the world influence their behaviours
and emotions when reacting to a situation. In general, an individual with various maladaptive beliefs
and attitudes becomes more vulnerable to depression because of his or her generalized negative
belief pattern.
Etiology of MDD– sociocultural factors
At this level of analysis, the focus is on the role played by social and
cultural factors in the development of MDD. According to the statistics,
after the age of 15, girls and women are twice as likely as boys and
men to be diagnosed with major depressive disorder (see Nolen
Hoeksema and Girgus, 1994). While biologists have pointed at
hormone differences related to the menstrual cycle as likely triggers for
depression, psychologists from the SCLOA have argued that adolescence for girls is a time of
restrictions on their choices and devaluation based on their gender. Coupled with the social
pressure on females to internalise feelings of anger and be unassertive in the face of challenges,
depression seems a likely outcome (Nolen Hoeksema and Girgus, 1994)
However, poverty and isolation have also been argued to be factors in the development of MDD.
Nicholson et al. (2008) found that men in the most economically and socially disadvantaged groups
in Poland, Russia and the Czech Republic were five times more likely to report depressive
symptoms than were richer citizens. Given that poor men and richer men share the same biology,
sociocultural factors could be assumed to play a relevant role here.
Diathesis-stress model applied to MDD
A diathesis-stress model of the etiology of mental disorder sees an interaction of biological, cognitive
and sociocultural factors as responsible for the disorder. For example, what we inherit from our
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parents is a genetic predisposition for MDD (biological). This would explain the high correlation for
MDD seen in identical twins. However, it is not a perfect correlation. As the studies examined earlier
showed, it is around 30% or 40%. Environmental triggers account for whether or not the inherited
predisposition results in mental disorder (sociocultural).
As well as biological predispositions which are triggered environmentally, Haeffel and Hames’
(2013) study of the new college students mentioned earlier shows that a stressful life event
(sociocultural) and a roommate who is cognitively vulnerable (sociocultural) can trigger cognitive
vulnerability (cognitive) in those predisposed to it. We will look further at the diathesis-stress model
when we consider the etiology of anxiety and eating disorders.
Study into sociocultural factors in the etiology of MDD
Chen et al. (2013) investigated the prevalence of depression in Chinese university students, and
identified several sociocultural factors associated with depression in this population.
A multi-stage stratified sampling procedure was used to select university students (N = 5245) in
Harbin (Heilongjiang Province, North-eastern China), who were aged 16–35 years. The Beck
Depression Inventory (BDI) was used to determine depressive symptoms of the participants, with
BDI scores of 14 or higher categorized as depressive. Depression was diagnosed by the Structured
Clinical Interview (SCID) of the Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition
(DSM-IV).
11.7% of the participants had a BDI score 14 or higher. Major Depressive Disorder was seen in
4.0% of these Chinese university students. There were no statistical differences in the incidence of
depression when gender, ethnicity, and university classification were analysed. Age, study year,
satisfaction with their course, family income situation, parental relationship and mother’s education
were significantly associated with depression. The students who were older, dissatisfied with their
course, had a lower family income, poor parental relationships, and a lower level of mother’s
education were susceptible to depression, with many of these suffering from MDD.
Principle that this study could be used to demonstrate
Culture (social norms and values) influences behaviour.
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ii. Etiology of anxiety disorders (post-traumatic stress disorder)
Post-traumatic stress disorder, often abbreviated as PTSD, is a
complex disorder in which the affected person's memory, emotional
responses, intellectual processes, and nervous system have all
been disrupted by one or more traumatic experiences. It is
sometimes summarized as "a normal reaction to abnormal events."
The etiology of post-traumatic stress disorder would seem at first
glance to be simple: a trauma. However, the
biological/cognitive/sociocultural debate is also relevant here, as
not everyone exposed to severe trauma develops PTSD, and
others who have not personally experienced a trauma, do.
Etiology of PTSD – biological factors
Because only a proportion of people exposed to traumatic events develop PTSD, it is important to
investigate the factors that increase the risk for the development of PTSD following trauma exposure
as well as the factors that might serve to protect individuals from developing this condition. Yehuda
(1999) argued that there are biological and familial risk factors for PTSD. His studies demonstrated
an increased prevalence of PTSD in the adult children of Holocaust survivors, even though these
children, as a group, had not been exposed to any unusual trauma. It is difficult, as Yehuda noted, to
disentangle the biological and sociocultural factors here; it may be that living with a parent who has
PTSD following their treatment during the Holocaust is enough to predispose children to developing
this, rather than any genetic connection.
More recently many neuroscientists are focusing on genes that play a role in creating memories of
fear. Understanding how these memories are created may help to find new interventions for
reducing the symptoms of PTSD. For example, PTSD researchers have pinpointed genes that
make:
•
Stathmin, a protein needed to form fear memories. In one study, mice that did not make stathmin
were less likely than normal mice to “freeze,” a natural, protective response to danger, after
being exposed to a fearful experience. They also showed less innate fear by exploring open
spaces more willingly than normal mice (Shumyatsky et al., 2005).
•
GRP (gastrin-releasing peptide), a signalling chemical in the brain released during emotional
events. In mice, GRP seems to help control the fear response, and lack of GRP may lead to the
creation of greater and more lasting memories of fear (Shumyatsky et al., 2002).
Researchers have also found a version of the 5-HTTLPR gene, which controls levels of serotonin —
a brain chemical related to mood-that appears to fuel the fear response (Hariri et al., 2002). Like
other mental disorders, it is likely that many genes with small effects are at work in PTSD.
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Study into biological factors in the etiology of PTSD
Uddin et al. (2010) used data from the Detroit Neighbourhood Health Study, a five-year project
funded by the National Institute of Health. They examined more than 14,000 genes using DNA from
blood samples provided by 100 Detroit residents. 23 of the participants suffered from PTSD and 77
did not.
The researchers identified numerous genes—most of them involved in regulating the immune
system—that appeared to be more active in people with PTSD. Previous studies have suggested a
link between altered immune function and PTSD. The new findings support that model and go a
step further by identifying a specific biochemical reaction that may be involved.
That biochemical reaction is a process called DNA methylation, and it can alter gene activity,
typically reducing it. Uddin et al. found that methylation levels of immune-related genes were lower
in the PTSD group, suggesting increased activity in those genes. That finding supports a model for
PTSD in which exposure to a traumatic event changes gene expression, which in turn alters
immune-system activity, leading to the disorder.
The findings have potential implications for the treatment of PTSD. Since DNA methylation states
are changeable, it's possible that genes identified in this study could become targets for new drug
therapies to treat PTSD.
Principle that this study could be used to demonstrate
There are biological correlates to behaviour.
Etiology of PTSD – cognitive factors
Researchers from the CLOA have identified the victims’ appraisal of the trauma at the time and
afterwards and their perception of the consequences, including others’ feelings towards them, as
vital cognitive factors in the onset and maintenance of PTSD. The central theme running through the
negative beliefs and appraisals is one of ongoing threat. Victims holding these types of negative
beliefs experience the traumatic event as continuing to have damaging implications, despite the
event being in the past. This continued threat then precipitates the anxiety at the heart of PTSD.
Themes of threat run through the global negative beliefs found to be associated with the onset and
persistence of PTSD. This can be related to the cognitive model of depression and cognitive
vulnerability discussed earlier.
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Study into cognitive factors in the etiology of PTSD
Dunmore et al. (1999) investigated the role of cognitive factors in both the persistence and onset of
PTSD. They studied patients' behaviour and emotional responses and appraisal of thoughts during
the traumatic event; and then in the posttraumatic phase the authors assessed posttraumatic
symptoms, other peoples' responses, and the perception of permanent impact of the trauma.
92 participants who were either physically or sexually assaulted at least three months prior to the
time of the study were included. The patients were given a PTSD symptom scale to evaluate current
symptoms and a rating based on their memories of the assault to evaluate symptoms just after the
assault. The patients were divided into groups. To assess onset factors patients who suffered PTSD
in the first month following trauma were compared to those who did not. To assess maintenance
factors patients who continued to experience PTSD were compared to those who had recovered.
In the PTSD vs. no PTSD group, cognitive tests showed that PTSD patients had:
Higher levels of mental defeat, confusion, and detachment during the assault
More negative appraisals of symptoms one month after
Perceived other people's reactions negatively
Belief that assault had permanent negative impact
Engaged in avoidance behaviour or attempted to undo memories
Negative beliefs both before and after occurrence
In the persistent PTSD vs. recovered PTSD groups, persistent PTSD patients had:
Higher levels of mental defeat
More negative appraisals of emotions, symptoms, and action
Engaged in avoidance behaviour or attempted to undo memories
More negative thoughts after the assault
This study was important in that it investigated the role of cognitive factors in both the persistence
and onset of PTSD. Since the study was retrospective some problems of interpretation are raised,
the authors suggest that further study is needed before it can be confirmed that cognitive factors can
confidently be used to predict the onset and persistence of PTSD.
Principle that this study could be used to demonstrate
Mental representations guide behaviour.
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Etiology of PTSD – sociocultural factors
In addition to the cognitive factors associated with PTSD, sociocultural
factors are also important. Cultural factors may modify the response to
trauma. Many cultures believe strongly in fate or accept the role of
divine intervention. These beliefs may lead to an acceptance of the
traumatic experience. Some Western techniques emphasize the need
for talking about the trauma as a means of recovery. This may be
forbidden in a culture that views discussion of a traumatic event as
inappropriate. For example, acknowledgement of an incident of rape
may be socially inappropriate in some cultures as it makes the victim
unmarriageable.
Lewis-Fernandez (2001) reported soldiers of Latino origin suffered
higher rates of PTSD after the Vietnam War compared to soldiers from
other ethnicities. Although this may be associated with factors such as
amount of exposure to combat or social isolation due to minority status, part of the difference has
been attributed to different rates of symptom reports among subgroups of Latinos. For example,
Puerto Ricans tend to report more symptoms in response to trauma than do Mexican Americans
(Ruef et al., 2000). Thus, variance in expressive styles may lead to artificially elevate rates of PTSD.
Alternatively, they may actually have higher posttraumatic effects. Further cultural analyses must be
performed to assess the validity of the various hypotheses.
Family and friendship factors may also affect risk. A history of family instability is associated with
increased prevalence of PTSD (King et al., 1996, in Halligan and Yehuda, 2000), whereas good
social support is associated with lower levels of symptoms (Solomon et al., 1988, in ibid).
Study into sociocultural factors in the etiology of PTSD
Brewin et al. (2000) conducted a meta-analysis of 14 separate risk factors for posttraumatic stress
disorder (PTSD), and the moderating effects of various sample and study characteristics, including
civilian/military status.
Three categories of risk factor emerged:
•
•
•
factors such as gender, age at trauma, and ethnicity predicted PTSD in some populations
but not in others
factors such as education, previous trauma, and general childhood adversity predicted
PTSD more consistently but to a varying extent according to the populations studied and the
methods used
Factors such as psychiatric history, reported childhood abuse, and family psychiatric history
had more uniform predictive effects.
Individually, the effect size of all the risk factors was small, but factors operating during or after the
trauma, such as trauma severity, lack of social support, and additional life stress, had somewhat
stronger effects than pre-trauma factors
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Principles that this study could be used to demonstrate
Culture (social norms and values) influences behaviour.
Human beings are social animals with a basic need to “belong”.
Diathesis – stress model applied to PTSD
The diathesis-stress model argues that people with an inherited or previously-acquired
predisposition towards PTSD could be predicted as being the most likely to suffer from the disorder
when placed in a traumatic situation. McKeever and Huff (2003) propose three causal pathways to
PTSD that interact to increase the likelihood: residual stress, ecological diatheses and biological
diatheses. In other words previous stressors (leading to residual stress) interact with environmental
and personal variables (ecological diatheses) and inherited traits, including neurological
abnormalities (biological diatheses) to produce PTSD. Here is a simplification of the model that they
suggest.
Biological
traits
PTSD
Ecological
variables
Cognitive
distortion
Residual
stress
iii Etiology of eating disorders (bulimia nervosa)
The symptoms of bulimia nervosa are given earlier in the section on prevalence. The only difference
between the DSM-IV and the DSM 5 when it comes to eating bulimia is that in DSM IV the bingeing
and purging behaviour had to take place at least twice a week. That has been reduced to once a
week in the DSM 5. (Note that the DSM 5 no longer uses Roman numerals in its title).
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Etiology of bulimia nervosa – biological factors
Researchers are still examining potential
biochemical or biological causes of bulimia
nervosa. There are all sorts of biological
abnormalities associated with bulimia, but
researchers in this area have been reluctant
to argue that biological correlates of bulimia
are actual causes of the disease, because
bulimia has the potential to disrupt
hormones and neurotransmitters, so that
biological changes may be just as likely to
be effects as causes. Indeed, many of the
anomalies are well-known effects of
starvation or stress, undermining their
causal possibilities.
Nonetheless, it is the belief of many
researchers that there is a genetic link to
eating disorders. Studies have
demonstrated that identical twins have a
greater co-occurrence of anorexia and
bulimia than fraternal twins. Identical twins
are more genetically similar than fraternal
twins, which supports the fact that eating
disorders have an inherited component.
Klump et al.’s (2000) reading of the twin-study literature led the researchers to conclude that 50–
83% of the variance in bulimia is genetic.
It has been found that some bulimia sufferers have imbalances in certain chemicals in the brain that
control hunger, appetite, and digestion. Investigation into the implications of these imbalances is still
underway. It has been shown that the neurotransmitters noradrenaline (norepinephrine) and
serotonin are severely diminished in patients that are suffering with acute cases of bulimia. These
are the same neurotransmitters that function abnormally when individuals are struggling with
depression. This correlation has led some researchers to suppose that there could be a link
between eating disorders and depression. In addition to creating feelings of emotional and physical
satisfaction, the neurotransmitter serotonin also is responsible for feelings of fullness after eating.
Also, the hormone cholecystokinin (CCK) has been shown to be diminished in women who are
struggling with bulimia. Similarly to the neurotransmitter serotonin, this hormone has caused
laboratory animals to experience fullness and stop eating.
Additional brain chemicals have been examined for their potential role in eating disorders. The
hormones cortisol and vasopressin have been observed at elevated levels in individuals with eating
disorders like bulimia nervosa and anorexia. Both cortisol and vasopressin are released in response
to emotional and physical stressors. Heightened levels of these hormones may be contributing
factors to some dysfunction experienced by individuals struggling with eating disorders. Other
research has indicated that individuals with bulimia and anorexia have heightened levels of the
hormones peptide-YY and neuropeptide-Y. Tests of laboratory animals have indicated that these
chemicals can stimulate eating behaviour.
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Levels of hormones and neurotransmitters in bulimia
Raised
Lowered
Cortisol (hormone)
Serotonin (neurotransmitter)
Vasopressin (hormone)
Dopamine (neurotransmitter)
Peptide YY (hormone)
Noradrenaline/norepinephrine (hormone)
Neuropeptide Y (hormone)
CCK (hormone)
Study into biological factors in the etiology of bulimia nervosa
Engel et al. (2007) conducted a meta-analysis of research into biological factors and eating
disorders and argued that inherited biological and genetic factors contribute approximately 56% of
the risk for developing an eating disorder. Individuals who have a mother or a sister with anorexia
nervosa are approximately twelve times more likely to develop anorexia and four times more likely
to develop bulimia than other individuals without a family history of these disorders. Studies of twins
have shown a higher rate of eating disorders when they are identical, compared to non-identical
twins or other siblings.
They also point to a lack of the neurotransmitter serotonin as being at least partly responsible for
bringing behaviour in people with bulimia nervosa. These individuals often crave (and gorge) on
foods rich in carbohydrates. The body converts sugars from carbohydrates, through a multi-step
process, into tryptophan. Tryptophan is then used to create serotonin, which is partially responsible
for the regulation of appetite, creating a sense of satiation, and regulating emotions and judgment.
Thus, the binge behaviour of bulimics may also be a response to low serotonin levels in the brain. A
research team at the University of Pittsburgh found that individuals successfully treated for bulimia
still had abnormally low serotonin levels, although other brain chemicals, such as dopamine and
norephinephrine, were normal in comparison to individuals with no history of eating disorders. The
successful treatment of bulimia with Prozac (a medication typically used for depression), which acts
to increase the amount of serotonin in the brain, is additional evidence of the importance of this
brain chemical.
Principle that this study could be used to demonstrate
There are biological correlates to behaviour.
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Etiology of bulimia – cognitive factors
Cognitive explanations for bulimia nervosa are very similar to cognitive
explanations for the development of MDD. There is a lot of overlap
between the two disorders, with “cognitive vulnerability” for one often
implying vulnerability for the other.
Themes of low self-evaluation, self-criticism, and distorted perception
of body size and weight are commonly found among people with
bulimia nervosa. Joiner et al. (1995) identified body dissatisfaction as a key factor in both MDD and
bulimia, and many studies since have agreed (see
http://guilfordjournals.com/doi/abs/10.1521/jscp.1995.14.4.339 for an extensive list).
Cooper et al. (2004) developed a sophisticated cognitive model of the development of bulimia, in
which relevant development factors include “negative early experiences, negative self-beliefs,
schema compensation processes, and different types of underlying assumption,” and relevant
factors maintaining the bulimic purging and eating cycle are “positive beliefs about eating, negative
beliefs about weight and shape, permissive thoughts, and thoughts of no control.”
Study into cognitive factors in the etiology of bulimia nervosa
Troop and Bifulco (2002) investigated whether certain difficulties in childhood are reported as
existing prior to developing an eating disorder.
Method: A sample of 43 women with a history of eating disorders and 20 women with no such
history were interviewed retrospectively about their feelings and experiences of loneliness, shyness
and inferiority in childhood and adolescence.
Results: Women with a history of anorexia nervosa of the binge/purge subtype reported higher
levels of loneliness, shyness and feelings of inferiority in adolescence than did women with no
history of an eating disorder, and women with a history of bulimia nervosa reported higher levels of
shyness. However, this was not true for earlier childhood where such feelings did not differ
significantly between groups. This difference could not be accounted for by current depressive
disorder, recovery from the eating disorder or level of victimization in adolescence.
Conclusion: There are a number of differences in the etiology of different eating disorders. The
present results suggest that cognitive styles pertaining to the social arena in adolescence, and prior
to the onset of any eating disorders, may play a causal role in the development of bulimia nervosa.
Principle that this study could be used to demonstrate
Mental representations guide behaviour.
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Etiology of bulimia – sociocultural factors
Sociocultural factors commonly reported as holding some responsibility
for the development of bulimia are unrealistic media images of “perfect
bodies”; sports that require a thin body (ballet, gymnastics, swimming;
family dynamics, including parents who are very weight-conscious and
focused on “perfection” and high achievement. Thinness becomes
equated with approval and success.
Keel and Klump (2003) argue that bulimia nervosa is a culture-bound
syndrome. They conducted research into bulimia nervosa in nonWestern cultures and found no studies reporting the presence of
bulimia in people with no exposure to Western ideals. All of the cases
involved individuals who were exposed to Western ideals and values
through urbanization, English-medium schools, previous residence in
Western nations, and/or higher socioeconomic status.
Study into sociocultural factors in the etiology of bulimia nervosa
Rodgers et al. (2009) examined a sociocultural model of the influence of parental comments on
body shape and eating concerns among males and females. Questionnaires were completed by 338
undergraduates. Participants reported levels of perceived parental comments, internalization of
media ideal images, appearance comparison, body dissatisfaction, drive for thinness and bulimia.
Results revealed that (regardless of gender) internalization and appearance comparison only
partially mediated the relationship between parental comments and the outcome variables. The final
model for females explained a larger proportion of the variability in body shape and eating concerns
than in males, with positive and negative parental comments directly related to body dissatisfaction
and through it to eating outcomes. In males, only negative comments were directly related to body
dissatisfaction. These findings highlight the role of parental influences in sociocultural models of the
development of body dissatisfaction and eating concerns, and the gender-specific patterns of
sociocultural influence.
Principles that this study could be used to demonstrate
Culture (social norms and values) influences behaviour.
Human beings are social animals with a basic need to “belong”.
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Diathesis-stress model of bulimia
The diathesis-stress model of bulimia looks at the interaction of biology, cognition and sociocultural
factors in the etiology of bulimia. Joiner et al (1997 – see above for their 1995 work on the overlap
between bulimia and MDD) developed a diathesis-stress model of the interrelations of perfectionism,
perceived weight status, and bulimic symptoms. The authors predicted and found that perfectionism
served as a risk factor for bulimic symptoms for women who perceived themselves as overweight
but did not serve as a risk factor for those who did not perceive themselves as overweight.
Perceived weight activated perfectionism as a predictor of bulimic symptoms; actual weight did not
serve the same role. This was true whether or not the women were actually overweight.
4. Implementing treatment
Learning outcome:
Examine biomedical, individual and group approaches to treatment.
Evaluate the use of biomedical, individual and group approaches to the treatment of one disorder.
Discuss the use of eclectic approaches to treatment.
There is a direct link between the beliefs regarding the etiology of disorders and the therapeutic
approach taken to treating them, which we will examine later. For now, we will explore the different,
and sometimes overlapping, therapeutic approaches to treating mental disorders.
A. Therapeutic approaches to treatment
i.
Biomedical approach to treatment
In line with the BLOA, and the belief that mental disorder is
caused by malfunction of the brain, especially involving
neurotransmission. Therefore, drugs or therapy that aims to
redress this insufficiency are the preferred biomedical approach.
MDD –
Drugs are used widely to treat MDD. There are three main
categories of drugs for MDD: two older groups - tricyclics and MAO-inhibitors are effective, but have
troublesome side effects & can be lethal if misused.
A biological theory that aims to explain MDD is the serotonin hypothesis, which suggests that there
is an inadequate amount of serotonin available in the synaptic gap between neurons for effective
transmission to occur. Based on the assumption from research that serotonin plays a role in
depression, medication for MDD increases serotonin. The most common group of drugs used
currently is the SSRIs, (selective serotonin reuptake inhibitors) which allow serotonin to remain for
longer in the synaptic gap, in order to be taken up by the receiving neurons and used, rather than
reabsorbed into the terminal button as excess. One of the most popular of the SSRIs is fluoxetine
(Prozac). The main criticism of any drug therapy is that it treats the symptoms, but does not cure
the disorder, and the medication needs to be continued for the effect to be maintained. Moreover,
many drugs have significant side effects that can outweigh the benefits felt from them, though it is
hard to commit suicide with SSRIs, unlike the earlier drugs.
It is difficult to assess the effectiveness of anti-depression medication, as we cannot k now what the
course of the MDD would have been if the patient had not taken the medication. One way is by
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trials comparing a group of patients who had taken medication for MDD and a control group who
had taken a placebo. Kirsch et al conducted a meta-analysis that suggested that there is only a
small difference in efficacy between taking a placebo and taking medication (2008, in Law et al.,
2010).
However, many new drugs are being investigated. One surprising candidate (except perhaps to
certain club-hoppers) is ketamine, an anaesthetic that's also sold on the street illegally under names
such as Special K. In a recent trial, it snapped people out of depression almost instantly, unlike
available medications that often take weeks to work (Berman et al., 2000) and it has been used in a
maintenance programme to produce long-term recovery (Messer and Haller, 2010). Ketamine acts
on different neurotransmitter receptors (glutamate, rather than serotonin) than current
antidepressants do. The problem is that it affects parts of the brain not related to depression, and
the drug can also cause hallucinations, so may not be suitable for all patients.
Electroconvulsive therapy (ECT)
This is a kind of psychiatric therapy that uses short electrical stimulus to the brain through tiny
electrodes in the temples. The charge lasts from 1 to 4 seconds and it causes epileptic-like seizures
to the patient. The patient is anesthetized and is given a muscle relaxant which would depress his
breathing. Oxygen will be given until they are able to normally breathe again. A majority of patients
would get 6 to 12 ECTs for a whole treatment, given one electrical charge per day, two or three
times in a week.
Electro-convulsive therapy is sometimes used for people with MDD for whom drug treatment fails.
Lapidus et al (2013) note that even now, a low-dose ECT treatment only to the right side of the brain
has an immediate anti-depressant effect, and higher repeat doses are not needed.
Both drugs and ECT are often more effective in combination with psychotherapy (see later for a
discussion of eclectic approaches to treatment of disorders).
Study into biomedical treatment for MDD
Duman and Aghajanian (2012) conducted research into the changes in the neurons and in the
synaptic gap during MDD. They conducted a meta-analysis of clinical studies that demonstrate that
depression is associated with reduced size of brain regions that regulate mood and cognition,
including the prefrontal cortex and the hippocampus, and decreased neuronal synapses in these
areas. Antidepressants can block or reverse these neuronal deficits, but typical antidepressants
have limited efficacy and delayed response times of weeks to months.
They comment that a notable recent discovery shows that ketamine produces rapid (within hours)
antidepressant responses in patients who are resistant to typical antidepressants. Basic studies
show that ketamine rapidly induces synaptic gap action and reverses the synaptic deficits caused by
chronic stress.
Principle that this study could be used to demonstrate
There are biological correlates to behaviour.
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PTSD –
Anti- depressant and anti-anxiety medication issometimes used to treat PTSD, again often in
combination with psychotherapy. In a meta-analysis of drug therapy for PTSD, Ipser and Stein
(2012) found that the SSRIs, as prescribed for MDD, had the most efficacy when compared to other
types of anti-depressant medication.
Andrade et al. (2011) note that ECT can also be used successfully on patients with PTSD. They
found marked improvement using 6 sessions of ECT over a period of 3 weeks, on 20 patients with
severe PTSD who had failed at least 4 antidepressant trials and at least 12 sessions of cognitive
behaviour therapy.
At the end of this section, we will evaluate the use of biomedical treatment for mental disorders.
Study into biomedical treatment for PTSD
Margoob et al. (2010) looked at treatment options for patients with severe, chronic, posttraumatic
stress disorder (PTSD). There is little information on the use of electroconvulsive therapy (ECT) for
PTSD. They treated twenty consenting patients with a fixed course of 6 ECT treatments
administered on an outpatient basis at a twice-weekly frequency.
Results: All but 3 patients completed the ECT course, and the result was statistically and clinically
significant improvement in the sample as a whole, and these treatment gains were maintained at a
4-6 month follow-up.
Conclusions: ECT may improve the core symptoms of PTSD independently of improvement in
depression, and may therefore be a useful treatment option for patients with severe, chronic,
medication- and therapy-resistant PTSD.
Principle that this study could be used to demonstrate
There are biological correlates to behaviour.
Bulimia nervosa –
Because bulimia is thought to be related to a lack of serotonin, in the same way the MDD is, SSRIs
are frequently used to treat bulimia. They are generally see as helpful, though there are reports that
they are more successful as a treatment for people with bulimia who also have the longer allele on
the 5-HTTLPR gene (see Monteleone et al, 2005). Again, they are usually used in combination with
psychotherapy.
ECT is used as a treatment for people with eating disorders, but often only when they are in tandem
with severe depression. (When you have one illness at the same time as another, this is called comorbidity).
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Study into biomedical treatment for bulimia nervosa
Mitchell et al. (2013) undertook a comprehensive review of drug therapy and other biological
treatments for eating disorders. Literature on this topic was systematically reviewed.
Results: The bulimia nervosa literature demonstrated the utility of antidepressants, particularly
SSRIs, in improving the symptoms of the disorder.
Discussion: The pharmacological treatment of eating disorders remains an underdeveloped field
although drug therapy clearly plays a role in the treatment of those with bulimia nervosa. Other
biological therapies have not been adequately studied
Principle that this study could be used to demonstrate
There are biological correlates to behaviour.
Evaluation of biomedical treatments –
MDD – there is a long history of treating MDD with different types of drugs. While some are
undoubtedly effective in reducing symptoms, there are also problems of addiction and side-effects,
and the criticism that they treat symptoms rather than the disorder itself are valid.
Strengths of biomedical treatment for mental disorders
If drug therapy or ECT succeeds in reducing the symptoms of psychologically-crippling mental
disorders then this in itself has to be seen as a huge advantage. Research suggests that in many
cases there is an alleviating of symptoms, especially when used in tandem with psychotherapy
(Cuijpers et al., 2010). For some people, just having a label to attach to their feelings, and being
told that medication might help, may be enough to make them feel somewhat better. In the case of
MDD, providing medication is continued for at least nine months after the symptoms have gone,
then the chance of relapse is greatly reduced.
Limitations of biomedical treatment for any of the mental disorders.
The anti-depressants prescribed for any of these disorders can be physically and/or psychologically
addictive. There are many documented side-effects, and most anti-depressant medication takes at
least four weeks to start working. They treat the symptoms, but unless the cause of the disorder is
addressed, it is likely that it will recur.
While ECT has been shown by many studies to reduce the symptoms of MDD, PTSD and bulimia
nervosa, there is still no clear picture of exactly how it works, which makes its use controversial. It
also has, usually temporary, effects on a person’s memory, which can be distressing. With regard to
the use of ECT, Read et al. (2004) note that almost half of the people receiving ECT are over 65
years old and by far the majority are female, up to 76% in Finland. This raises questions of how
people are selected for this treatment.
The biomedical approach is reductionist and fails to take a holistic approach, instead focusing on
particular neurotransmitters. MDD can be a symptom of something very wrong in a person’s life that
will not be immediately apparent and may take long sessions of therapy to uncover. According to
Halligan (2007) it is crucial to take a biopsychosocial, rather than a biomedical, perspective and
reject the belief that illness is the result of discrete biological processes. Instead illnesses and
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mental disorders can be meaningfully explained in terms of cognitive and sociocultural factors, and
consideration of these has to form part of the treatment.
ii. Individual approaches to treatment
MDD Cognitive-behavioural therapy (CBT) is the most common individual
treatment for MDD. Cognitive- behavioural therapy (CBT) is a term that
encompasses numerous specific treatment approaches. As the name
suggests, cognitive-behavioural treatments incorporate both cognitive
and behavioural strategies. With regard to depression, CBT refers to
the use of both cognitive restructuring and the behavioural strategy of
activity scheduling or behavioural activation. In other words, it
addresses the underlying negative thoughts that lead to the depression
and helps the person see that these thoughts are faulty and are
responsible for their emotional state.
Beck and Weishaar believe that in order to treat MDD, clients need to treat their faulty
interpretations and conclusions as testable hypotheses. The role of the therapist in a cognitivebehavioural intervention is to help the clients examine alternative interpretations and to produce
contradictory evidence in order to move to cognitive restructuring, whereby the client revises and
replaces his/her faulty thoughts and beliefs. It is the thought that counts.
Study into individual CBT for MDD
Siddique et al. (2012) undertook a study of 267 low-income young minority women, with either
moderate or severe depression, comparing the treatment outcomes after one year on medication or
one year of CBT.
They found that among depressed women with moderate baseline depression medication was
superior to CBT at 6 months, but the difference was not sustained at 1 year. Among women with
severe depression, there was no significant difference between the two groups at 6 months, but
CBT was superior to medication at 1 year.
Principle that this study could be used to demonstrate
Mental representations guide behaviour.
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PTSD –
Individual therapy, especially cognitive behavioural therapy, has been shown to be effective in
treating PTSD, leading people to turn their hopelessness into the belief that “that which does not kill
you makes you stronger”.
Specific techniques in therapy for PTSD include exposure and cognitive restructuring. Other
techniques, such as relaxation, self-talk and assertiveness training may also be used. Exposure
therapy involves gradually facing the thoughts and memories of the traumatic event or situations
(places where the event occurred) that make one anxious. This can be done by using imaging
techniques or by actually returning to the place where one had an accident. Exposure should be
gradual and done with the help of an experienced clinician.
Exposure therapy is intended to help the client face and gain control of the fear and distress that
was overwhelming in the trauma, and must be done very carefully in order not to re-traumatize. In
some cases, trauma memories or reminders can be confronted all at once (“flooding”), while for
other individuals or traumas the therapist will work gradually up to the most severe trauma by using
relaxation techniques and either starting with less upsetting life stressors or by taking the trauma
one piece at a time (“gradual desensitization”).
Cognitive restructuring involves identifying irrational (but understandable) patterns of thought, feeling
and behaviour that emerge after a traumatic event. The person gradually learns to substitute new
thoughts, such as replacing mistrust of everyone with trust of those closest to us, and then gradually
extending this circle of trust.
Smith et al. (1999, p 177) note that CBT often encompasses diverse elements such as problem
solving strategies, cognitive restructuring of thoughts, skills teaching, and behaviourally-based
exposure. They note that CBT, especially when taken in its broadest sense, is effective treatment for
PTSD, but in the case of children and adolescents, additional work with parents is also
recommended.
Study into individual CBT for PTSD
Murray et al. (2013) examined individual therapy for young people who experience ongoing traumas.
Trauma-focused cognitive–behavioural therapy (TF-CBT) is an evidence-based treatment that has been
used successfully with youth and families who experience ongoing traumas. Within these studies and
projects, TF-CBT trainers worked collaboratively with young people, families, and service providers to
develop TF-CBT strategies to best respond to populations with continuous trauma. They concluded that
research suggests that even in cases of continuous traumas, youth can be treated with TF-CBT and they
will improve significantly.
Principle that this study could be used to demonstrate
Mental representations guide behaviour.
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Bulimia nervosa Like CBT for PTSD sufferers, CBT for people with bulimia will focus on identifying and altering
dysfunctional thought patterns, attitudes and beliefs, which may trigger and perpetuate the person’s
pattern of harmful eating behaviours. CBT used in the treatment of bulimia focuses on the traditional
foundations of CBT therapy — helping a person understand, identify and change their irrational
thoughts (the “cognitive” part), and helping a person make the changes real through specific
behavioural interventions (such as promoting health eating behaviours through goal setting,
rewards, etc.). Although the results of the study below show that CBT is not consistently better than
other forms of therapy, such as psychoanalysis, CBT therapists point out that it takes less time to
produce improvement, and is a lot less expensive than most other therapies.
Study into individual CBT for bulimia nervosa
Wilson et al. (1993) conducted a meta-analysis into research regarding the use of CBT in the
treatment of bulimia nervosa. CBT is designed to alter abnormal attitudes about body shape and
weight, replace dysfunctional dieting with normal eating habits, and develop coping skills for
resisting binge eating and purging.
The researchers concluded that CBT is effective in reducing all core features of BN and shows
good maintenance of therapeutic improvement. Although superior to therapy with antidepressant
drugs, CBT has not been shown to be consistently superior to alternative psychological treatments.
Different hypotheses about CBT's mechanisms of action remain to be investigated.
Principle that this study could be used to demonstrate
Mental representations guide behaviour.
Evaluation of individual approaches to treatment
As cognitive-behavioural therapy is the preferred individual approach for all three mental disorders
discussed in this chapter, it is on this that the evaluation will focus.
Strengths of individual CBT for any of the mental disorders
The CBT model has great appeal, because, unlike biomedical treatments, it puts control in the
hands of the client, rather than the psychologist or psychiatrist. Cognitive theories lend themselves
to testing, as many people with psychological disorders, particularly depressive, anxiety, and sexual
disorders have been found to display maladaptive assumptions and thoughts and cognitive therapy
has been found to be very effective for treating many types of mental disorders (Beck et al.,1989).
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Limitations of individual CBT for mental disorders
The maladaptive cognitions seen in psychologically disturbed people could be a consequence of
their mental disorder, rather than a cause. The cognitive model is narrow in scope - thinking is just
one part of human functioning, and maybe broader (biological and/or sociocultural) issues need to
be addressed. For people who have difficulty expressing themselves verbally, CBT may prove
impossible.
iii. Group approaches to treatment
Just as the biomedical and individual approaches can be seen to be
directed by the principles of thought underlying the BLOA and the
CLOA respectively, so the group approaches to treatment owe a lot to
the principles of the SCLOA.
Cognitive-behaviour group therapy (CBGT) may be defined as therapy
that uses the dynamics of the group format, in addition to the common
cognitive behavioural therapy techniques to change distorted, maladaptive, and dysfunctional
beliefs, interpretations, behaviours, and attitudes (Bieling et al., 2006)
MDD –
The theory behind group therapy for MDD is that people may feel more compelled to engage in
group discussion than they are when alone with a therapist. They may also learn from hearing about
the experiences of others in similar circumstances. If through the group they meet others who have
recovered or improved, they may also feel more hopeful about their own chances of doing the same.
CBGT has been shown to be effective in residential settings, as well as in outpatient clinics. Watkins
et al (2011) found that CBGT was an effective treatment for major depression for clients in
residential substance abuse treatment, resulting in a decrease in symptoms of depression and a
decrease in substance abuse after discharge.
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Study into group CBT for MDD
Clarke et al. (1999) examined the effectiveness of cognitive-behavioural therapy (CBT) for
depressed adolescents.
Method
Adolescents with major depression (N = 123) were randomly assigned to 1 of 3 eight-week
conditions: adolescent group CBT (16 two-hour sessions); adolescent group CBT with a separate
parent group; or control on a waiting list. Subsequently, participants completing the CBT groups
were randomly reassigned to 1 of 3 conditions for the 24-month follow-up period: assessments
every 4 months with extra (“booster”) CBT sessions; assessments only every 4 months; or
assessments only every 12 months.
Results
The CBT groups yielded higher major depression recovery rates (66.7%) than the control (48.1%),
and greater reduction in self-reported depression. Outcomes for the adolescent-only and
adolescent + parent conditions were not significantly different. Rates of recurrence during the 2year follow-up were lower than found with treated adult depression. The booster sessions did not
reduce the rate of recurrence in the follow-up period but appeared to accelerate recovery among
participants who were still depressed at the end of the acute phase.
Principle that this study could be used to demonstrate
Cognitive processes are influenced by social and cultural factors.
(This is a CLOA principle, but is the best fit here.)
Human beings are social animals with a basic need to “belong”.
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PTSD –
Group CBT for PTSD is recommended by many psychologists. Beck and Coffey (2005) admit that it
is often time and reimbursement issues that lead practitioners to recommend group therapy, but the
method has a number of advantages over individual CBT. The other attendees, for example,
constitute a natural support group and there is the ability to reach more patients. Moreover, the
results are equally as good as those for individual therapy.
Study into group CBT for PTSD
Giannopoulou et al. (2006) examined the effects of a short-term group cognitive-behavioural
intervention in children who were experiencing PTSD symptoms following the Athens 1999
earthquake.
Method - Twenty children, aged 8-12 years, referred for treatment to a local child mental health
team were assigned to two groups - Group 1 ( N = 10), which started treatment 2 months after the
earthquake and Group 2 ( N = 10), which started treatment at 4 months post-earthquake.
Results - A statistically significant reduction in overall PTSD symptoms - intrusion, avoidance, and
arousal - as well as in depressive symptoms was reported immediately after the intervention. The
treatment also produced a statistically significant improvement in children’s social functioning.
Further significant improvement was reported in children at an 18-month follow-up. Treatment
gains were maintained at a 4-year follow-up.
Conclusions - Despite several limitations to this study, short-term group CBT (cognitivebehavioural therapy) was found to be a useful treatment approach, which can be offered in clinical
settings, particularly if resources are limited.
Bulimia nervosa –
Group therapy is common for eating disorders, including bulimia. A study by Woodside and Kaplan
(1994, in Law et al., 2010) put males and females together in group therapy that specifically targeted
negative and destructive attitudes to eating. The results were an improvement in eating attitudes.
For the same reasons as given before (increased hope when seeing others’ improvement and
access to a natural support group) CBGT is seen as helpful for those with bulimia. However, some
therapists prefer family therapy as a bridge between individual CBT and group CBT: the family can
give support after individual CBT without exposing the sufferer to the possibility of learning
strategies to avoid weight gain from other group members (see the evaluation of group therapy later
in this chapter).
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Study into group CBT for bulimia nervosa
Chen et al. (2003) investigated if results of group and individual CBT for bulimia are clinically
comparable.
Method
Sixty patients with bulimia from hospitals and general practitioners in Sydney, Australia, were
allocated randomly to group or individual CBT. Forty-four completed treatment (22 in group
CBT and 22 in individual CBT). Patients were assessed at pre-treatment, post-treatment, and
at 3 and 6 months follow-up, examining weight and shape attitudes, social adjustment, selfesteem and general psychopathology.
Results
The effects of group and individual CBT were equivalent on most measures. However, a
significantly greater proportion of individual CBT patients than group CBT patients were
abstinent from bulimic behaviours at immediate post-treatment, but not at the 3 month and 6
month follow-up.
Agras et al (2000) compared CBGT with inter-personal therapy (targeted personal therapy with a
mental-health professional) and found that CBGT was significantly more rapid in engendering
improvement in patients with bulimia nervosa than IPT. They concluded that CBGT should be
considered the preferred psychotherapeutic treatment for bulimia nervosa.
Evaluation of group approaches to treatment
As group cognitive-behavioural therapy (CBGT) is the preferred group approach for all three mental
disorders discussed in this chapter, it is on this that the evaluation will focus.
Strengths of CBGT for any of the mental disorders
Consistently good outcomes have been recorded for CBGT in comparison with, and sometimes in
addition to, other forms of intervention. The skills learnt are useful, practical and helpful strategies
that can be incorporated into everyday life to help sufferers cope better with future stresses and
difficulties. Being in a group with people in the same position can help the person with the mental
disorder feel less isolated and more hopeful of recovery or improvement. Group support can actually
make the prospect of recovery a reality. CBGT is relatively quick (usually up to about 12 weeks in
duration) and less expensive than other therapy.
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Limitations of CBGT for any of the mental disorders
Imitations of this method include the risk of one patient monopolizing therapy, confrontation between
group members, and the development of subgroups. Group settings may also make group members
more reluctant to discuss disturbing cognitions, and as a result of this fail to undertake and
challenge these maladaptive thoughts (Morrison, 2001, Yalom, 1995). Patients who are severely
depressed or traumatized may not be able to participate.
With CBGT for eating disorders, there is a risk that being in a group of similarly bulimic patients
lends legitimacy to a new identity based on the group membership, which reinforces the undesired
eating patterns. Members of the group may also teach each other, albeit unintentionally, strategies
to avoid weight gain (Polivy, 1981, in Law et al., 2010).
iv. The eclectic approach to treatment
An eclectic approach is an approach that combines two or more
techniques for treatment. The treatment is adapted to suit the needs of
the individual or group. Sometimes patients receive drug therapy in
combination with psychotherapy, and half of all therapists describe
themselves as taking an eclectic approach (Myers, 2010). Many
combinations are possible, but the most common is drug and
psychotherapy (usually CBT) combined.
There are different types of eclectic approach. The most common is
simultaneous use, which is use of the therapies at the same time. Sequential use is when one
therapy follows another, and stage-oriented use is when one therapy is used at the critical stage and
other(s) are introduced at the maintenance stage. Stage-oriented therapy often involves drug use to
stabilize behaviour and emotions so that the person may benefit from CBT at the maintenance
stage.
Lebow (2002) gives a list of advantages of the eclectic approach that it is worth paraphrasing here:
•
•
•
•
•
•
an eclectic approach has a broader theoretical base, and therefore may be more
sophisticated than an approach using only one theory.
there is greater flexibility offered to the client, and individual therapy needs may be met.
there is more chance of finding an effective treatment if two approaches are used in tandem.
this approach is suitable for a wider range of clients than a single approach.
a therapist using an eclectic approach is not biased towards one treatment theory and
method, and therefore may be more objective.
a therapist using an eclectic approach can revise and rebalance treatment according to
which approach appears to be most effective.
However, he warns that the eclectic approach should not be the same as having no clear idea of what
would work and nor should it be applied inconsistently. Sometimes the approach is too complex for
one therapist to undertake, and finally all treatment, eclectic or not, should only be used if backed up
by evidence from previous studies that it works.
Petersen (2007) writes that drug/psychotherapy combinations are useful, so long as the two are
combined in specific ways. Recent research (Fava et al., 2005) has suggested that sequential
administration of antidepressant and psychotherapeutic treatments, with the therapy coming after the
acute-phase drug response, may be more protective against relapse and recurrence than
simultaneous treatment.
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B. The relationship between etiology and therapeutic approach
Learning outcome
Discuss the relationship between etiology and therapeutic approach in relation to one disorder.
Because discussion is easiest using the following models and explanations for MDD, it is on this that
we will focus.
MDD – relationship between biological (neurotransmitter-focused) explanations and
treatment with SSRIs.
The principle that there are biological correlates for human behaviour,
including moods and emotions, is behind the most common biomedical
theory of the etiology of MDD. This is the theory that brain
neurochemicals are responsible for human depression and therefore
any treatment should be focused in this area.
Although there is no real clear picture concerning how depression might
develop biologically, many theories have centred on the hypothesis that
the transmission and reuptake of neurotransmitters, especially
serotonin, dopamine and noradrenaline, underlies depression. These
neurotransmitters are known collectively as the catecholamine
neurotransmitters, or sometimes as monoamine oxidase [MAO]
transmitters. This theory was proposed in the mind-1950s, after researchers found that drugs that
affected the release and breakdown of these transmitters had varying effects on mood (Gross, 2010
p 708). This was a huge turning-point as previous treatments for depression had often involved long
periods in mental institutions, undergoing such treatments as insulin comas, ECT or “sleep cures”.
(See Lopez-Munoz and Alamo, 2009, for a fascinating history of the treatment for depression).
In 1965, Schildkraut put forth the hypothesis that depression was associated with low levels of
noradrenaline, and later researchers theorized that serotonin was the neurotransmitter of interest
(Coppen et al., 1967). The (rather reductionist) theory that depression was caused by a lack of
certain neurotransmitters, led to the development of anti-depressant drugs, hailed as A large
amount of research demonstrated the effectiveness of a new drug, fluoxetine (marketed initially as
Prozac) that was developed in 1988 as a replacement for the older anti-depressants (tricyclics and
monoamine oxidase inhibitors [ MAOIs]) that targeted the enzyme monoamine oxidase, preventing it
from breaking down the neurotransmitters, and so allowing them to remain active in the synaptic gap
for longer.
Fluoxetine and similar drugs are selective/specific serotonin reuptake inhibitors. Because they have
been successful in treating MDD, a stronger link has been established between low levels of
serotonin and depression (Davison and Neale, 2001).
However, although the “neurochemical” theory of depression is the longest-standing of the biological
theories (others are evolutionary theory and brain structure theories) and the main anti-depressants
have an effect on levels of serotonin and noradrenaline, by the time the drugs’ effects are felt (which
can be about 4 weeks) the levels have returned to their previous level, even though the patient is
feeling better. So the lack of serotonin and adrenaline cannot be as directly implicated in the mood
disorder as claimed (Gross, 2010, p 708).
Moreover, Lacasse and Leo argue that there is no baseline “normal” level of serotonin against which
to measure a depressed person’s levels, and just because aspirin cures a headache, this does not
mean that the headache was caused by a lack of aspirin (2005, p 1212). Levinson (2006) notes that
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the short allele on the 5-HTT gene acts the same way as Prozac – it prevents the reuptake of
serotonin, but people with the short allele on this gene are more likely to suffer from depression.
This means that a possible cause of depression and a possible cure for depression actually act the
same way.
Therefore, it would be correct to assume that a lot more investigation needs to be undertaken into
this area.
MDD – relationship between cognitive theories of depression and CBT
The cognitive principle that mental representations guide behaviour,
and therefore manipulation of these representations will have
corresponding effects on behaviour, underpins CBT treatment for MDD.
Beck found evidence that "deviation from logical and realistic thinking
was found at every level of depression from mild neurotic to severe
psychotic" (1967, p 240). He devised the negative cognitive triad to
explain what people with MDD experience:
•
•
•
Depressed people see themselves as inadequate, incapable of success, and always as a
victim of circumstances.
They consider all past and present experiences through the kaleidoscope of negativity,
constantly emphasizing on defeats, failures, and a victim mentality.
They view the future in the same way, seeing only despair and hopelessness.
Beck laid major emphasis on understanding and changing core beliefs as an approach to treating
depression. His CBT was developed as an alternative to psychodynamic psychotherapy, the
offshoot of psychoanalysis whose main function was the treatment of neurosis, largely what today
are called anxiety disorders. By restructuring negative thinking, he believed that positive changes
could be made in the depressed client. He considered the role of a therapist as crucial in the
treatment. The therapist involves the client in setting realistic goals and taking responsibilities for
action and thought. By changing thought and perception, a change can be brought in behaviour and
emotional responses. A course is outlined to educate the client on the concept of faulty thinking.
New ideas and ways are generated to develop a positive outlook of oneself, experiences and the
environment around. Sometimes, home assignments are also given to help the depressed person
review and understand the impact of faulty thinking on behaviour and emotional well-being.
Today psychologists use his theory, and the scales that he developed for measuring depression, in
CBT for those with MDD. But studies confirming the efficacy of CBT have been criticised for a lack
of rigour (Kramer, 2008). One of the most enduring criticisms of CBT is that it does not put enough
emphasis on a person’s emotional life. CBT theory contends that what you feel is somehow not very
important to why you do what you do and think what you think. It has been described as Rowe
(2008) as a “quick fix” that simplifies the assault to the sense of self that lies at the heart of mental
distress.
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MDD – relationship between the psychosocial (vulnerability) model and group therapy
The principle underpinning the psychosocial model is that human
beings are social animals with a basic need to belong. The
psychosocial model of the etiology of depression developed by Brown
and Harris (1978) proposes several "vulnerability factors"--namely early
maternal loss, lack of a confiding relationship, more than three children
under the age of 14 at home, and unemployment--can interact with
"provoking agents" to increase the risk of depression. Writing much later, Harris (2001) comments
“recent studies have traced the well-known gender difference in depressive prevalence to
differences both in gender role involvement with the provoking life events and in styles of supportseeking/support-giving. What emerges is the powerlessness, loss and humiliation characterising the
final pathway [to depression].”
Social support, both within and outside the home, is seen as helping the depressed person to
improve. Ideas concerning the preventive and curative role of social support have been the prime
inspiration of many psychosocial interventions reported. Group therapy in a well-functioning group
can replace a lack of family support and enable people to build healthy relationships and improve
their feelings of self-worth through non-judgemental communication. With more and more people
living alone or feeling isolated, the popularity of psychosocial support groups has increased.
Cramer et al (2011) conducted a study into using CBGT for treating women with depression and
concluded that it was effective. However, critiques of the effectiveness of group therapy in treating
MDD have focused on its ineffectiveness with the most serious cases of depression, and the fact
that the reports of its success have often been from studies that were not well-controlled, so as such
remain anecdotal (Huntley et al., 2012).
______________________________________
The key to understanding the arguments regarding Abnormal Psychology is not to see them in
isolation. There is a theoretical relationship between perceived etiology, estimated prevalence and
recommended treatment for each of the disorder studied.
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