lecture 4 - mental health disorders 2 Flashcards
eating disorders in DSM5
Anorexia nervosa – ‘lack of appetite due to nervousness’
Bulimia nervosa – ‘could eat an ox’ - due to nervousness
about eating strange things and control of eating
10 types of feeding and eating disorders in DSM -
pica in children
pica in adults
rumination disorder
avoidant/ restrictive food intake disorder
anorexia nervosa restricting type
anorexia nervosa, binge eating/ purging type
bulimia nervosa
binge-eating disorder
other specificied feeding or eating disorder
unspecified feeding or eating disorder
pica
Pica is the consumption of substances with no significant nutritional value such as soil, soap
or ice.
Subtypes are characterized by the substance eaten
Acuphagia (sharp objects)
Amylophagia (starch)
Cautopyreiophagia (burnt matches)
Coniophagia (dust)
Coprophagia (feces)
Emetophagia (vomit)
Geomelophagia (raw potatoes)
Geophagia (dirt, soil, clay)
Hyalophagia (glass)
Lithophagia (stones)
Mucophagia (mucus)
Pagophagia (ice)
Plumbophagia (lead)
Trichophagia (hair, wool, and other fibres)
Urophagia (urine)
Hematophagia (Vampirism) (blood)
Xylophagia (wood, or derivates of wood such as paper)
This pattern of eating should last at least one month to meet the diagnostic criteria of pica.
way to cope with stress, displacement mechanism
Normal BMI
But leads to
Malnutrition
Lead poisoning
Stomach problems
Iron deficiency etc
physiological problems as a result of psychological problems
anorexia nervosa - anxious eatig
Major issues
reduced food intake
‘fear of becoming fat’ and
refusal to maintain minimal weight
no lack of appetite
preoccupation with food
intense fear of obesity
high mortality rate (suicide)
Low BMI
Medical complications
cold to touch/bluish skin colour
poor temperature regulation
low BP/feel weak, dizzy
heart arrhythmia – hypokalemia
electrolyte imbalance/kidney damage
Vitamin (B1) deficiency/depression
hair thinning/brittle skin
downy hair growth on body
bulimia nervosa
Major issues
loss of control of food intake
‘fear of becoming fat’
binges/gorging
purging/exercise
concern with body shape
Normal (may be high) BMI
Medical complications
electrolyte imbalance/kidney damage
Vitamin (B1) deficiency/depression
heart arrhythmia – hypokalemia
heart muscle damage
throat/mouth damage - due to stomach acid etc
dental damage
mouth ulcers
swollen glands
Eating disorders – body morphing
Tovee et al., 2003
AN have lower BMI (and lower ideal BMI)
AN and BN overestimate size of their bodies
people with eating disorders misjudged body size
looked at percentage difference between guess and actual body size
eating disorders - an inetrnational perspective
Becker et al 2002
eating behaviours and attitudes following prolonged exposure to TV among ethnic Fijian adolescent girls
a score greater than 20 indicated an eating disorder
used EAT-26 scores - survey for eating issues
media influences eating patterns - eating disorder could be a product of modern time however prevalence could have increased
not just a modern disease
13th & 14th Century: practice of self-starvation – piety and purity
15th Century: Mary, Queen of Scots – detailed medical history
weight loss, diarrhoea, pallor, fainting
17th Century: Morton:
.. and the Eighteenth year of her Age, in the month of July, fell into a total suppression of her Monthly Courses from a
multitude of Cares and Passions of her Mind, but without any of the symptoms of the Green-Sickness following upon it… her
appetite began to abate, and her Digestion to be bad; her Flesh also began to be flaccid and loose, and her looks pale, with
other symptoms usual in a Universal Consumption of the Habit of the Body.
19th Century: Sir William Gull: “Anorexia Nervosa” paper
At present our diagnosis is mostly one of inference, from our knowledge of the liability of the several
organs to particular lesions; thus we avoid the error of supposing the presence of mesenteric disease in
young women emaciated to the last degree through hysteric apepsia, by our knowledge of the latter
affection, and by the absence of tubercular disease elsewhere.
It will be noticeable that as she recovered she had a much younger look, corresponding indeed to
her age, twenty-one; whilst the photographs, taken when she was seventeen, give her the
appearance of being nearer thirty
eating disorders - aetiology
Biological factors – high genetic incidence – run in families, high concordance in MZ twins
alterations in cerebral serotonin levels/function – use of SSRIs
link to changes in oestrogen (incidence during puberty)
Family influences – parental pressures/comments on appearance/food intake/abuse
Sociocultural factors – peer and media influences – Western culture
the internet
Individual drives – idealising thinness - Barbie doll, Miss World, actresses, pop stars
(AN+BN) body dissatisfaction – aim to be thin – media drive
perfectionism – linked to ideal of thinness – want ‘perfect’ body
dieting – general start point – aim to lose weight
dieting=dissatisfaction, failure to achieve= negative affect
negative affect – risk factor for body dissatisfaction
self-criticism
binging=feel better, but need to purge (downward spiral)
eating disorders - treatment
Anorexia
Poor response to treatment – pessimistic view of effect
if condition worsens – forced feeding
No reliable medical intervention – SSRI treatment helps with disturbed thinking
Family therapy – treatment of choice – especially adolescents
Cognitive behavioural therapy – modifying distorted beliefs
Bulimia
Medications – anti-depressants (SSRI) for associated depression
decrease binge frequency +disturbed thinking
Cognitive behavioural therapy – treatment of choice
Early intervention predictive of greater success (Fairburn et al., 2004)
needs some kind of management or therpay as parents not aware they are doing anything wrong
early intervention is better
gene/ environment/ diathesis / stress
nature or nurture
nature - biological factors - genes, proteins, neurotransmitters - normal/ abnormal behaviour trait function
nurture - enviroenmtal factors learning experiences parenting childhood trauma what you eat - normal/abnornmal behaviour trait function
aetiology - key concepts
Biological/medical model
Psychoanalytical model
Behavioural model
Cognitive model
The biological/medical model
Basic tenet: pure medical or physiological cause
Mental disorder = physical disease
Types of condition:
Depression Schizophrenia
Substance abuse Eating disorders
ADHD OCD
Types of treatment?
Pharmacology – anti-psychotic drugs
- anti-depressant drugs
- anti-anxiety drugs
- mood stabilising drugs
Neurosurgery Deep brain stimulation - helps part of the brain function - electrodes used for parkinosons
Gene therapy - if we know theres a genetic mutations may be able to replace the damaged gene - conditions can be passed on genetically
Phineas gage - damaged prefrontal cortex - behaviour and personality changes
Pros and Cons
Pros
Heredity of conditions
Definite treatment routes - Pharmacology
Cons
Many disorders have no clear cause … - no single gene change or biological changes the cause - its Moree than just biology
Few conditions 100% penetrant
Psychoanalytic viewpoint
Unresolved conflicts/trauma in childhood – haunt adulthood
Locked in unconscious mind
Unconscious issues affect conscious thoughts/actions - conflict
Leads to irrational/maladaptive behaviour
Development of different aspects of personality/drives at different stages of life
Need to progress through stages – correct levels of gratification
Types of condition?
Anxiety – neurotic conditions
Stress
Mood
Developmental disorders
Treatments?
Psychoanalysis/therapy
Pros and Cons
Pros
Idea of developmental issues – distal events
Latent effects in childhood, showing in
adulthood – predisposition
Cons
Does not consider current issues of patient
i.e. adult
Not scientifically grounded
behaviourist viewpoint
Types of condition?
Phobias
Gambling
Addiction
Types of treatments?
Behavioural therapy - to alter the learning situation - exposure therpay eg flooding
Desensitisation - cab do in controlled virtual environment - provide good post conditioning experience
Modelling
Motivation/rewarded behaviours
Behaviour determined mainly by environment
Exposure to different environments = different
learning experiences
Abnormal behaviour = maladaptive forms
learned through experience
Failure to learn ‘normal’ adaptive behaviours
Or learning of ‘wrong’ behaviours
Conditioning
we associate things and learn from what other people are doing
Pros and Cons
Pros
Highlights role of learning in behavioural
expression
Cons
Implies pure environmental aetiology
Little evidence of the conditioning experience
the cognitive model
Types of conditions?
Phobias
Anxiety
Depression
Personality disorders
Types of treatments?
Cognitive-behavioural treatment (CBT) - restricting schemas and thought processes
Information processes – attention, memory,
thinking, planning
Internal reinforcement
Schema – representation of knowledge,
Expectations, roles, people, events
Self-schemas – views on self - an get distorted
Can be strongly held/represented
Distorted/inaccurate schemas – poor learning
Pros and Cons
Pros
Step up from behaviourism - thoughts
Highlights mental processing
Distorted thoughts lead to illness
Cons
Implies pure environmental aetiology
approaches to abnormal psychology
What are the causes of disorders? (or reasons for our behaviours/traits?)
Is our behaviour all intrinsic – biological? Or all extrinsic – environmental?
Or Proportion of both? Are we born with a predisposition?
Is there a specific cause of specific condition? Note that many different treatments effective
May be a mix of factors – intrinsic predisposition + extrinsic stressor and vice versa
“most disorders are the result of many causal factors—biological, psychological, and
sociocultural—interacting with one another. Moreover, for any given person, the particular
combination of causal factors may be unique,or at least not widely shared by large numbers
of people with the same disorder” (Hooley book, p117)
Depending on who is using this “model”, depends on where the emphasis lies!
diathesis - stress
diathesis
n. (pl. -ses ) congenital susceptibility or aptitude; predisposing factor. diathetic,, a
does not have to be biological can be environmental
diathesis + stressor = disorder
diathesis + 0 =/ disorder
0 + Stressor =/ disorder
need both
diathesis (more senstive eg PTSD) + stressor = disorder
diathesis (less sensitive) + stressor (strong stressor or a series of stressors) = disorder
the relative impact of these things varies in each individual
predisposition could be event from past hidden
need predisposition and something later in life - stressor
Nature or Nurture?
Biological
factors
Genes, proteins, neurotransmitters —-> diathesis ——> Environmental
factors
Learning experiences, parenting, childhood trauma
what you eat…
—> behaviour trait function
levels of explaination
Global
Cultural
Social
Psycho-
logical
Neuro’
Gene-
tics
necessary, sufficient and contributory causes of abnormal behaviour
A necessary cause
(X) is a characteristic that must exist for a disorder (Y) to
occur. For example, general paresis (Y)—a degenerative
brain disorder—cannot develop unless a person has previ-
ously contracted syphilis (X). Or more generally, if Y
occurs, then X must have preceded it. Another example is
Huntington’s chorea—a rare degenerative brain disorder
of the central nervous system—which can develop only if
the person has the necessary gene (IT15, or the Hunting-
ton’s gene—see Chapter 14). To date, most mental disor-
ders have not been found to have necessary causes,
although there continues to be a search for such causes.
A sufficient cause of a disorder is a condition that
guarantees the occurrence of a disorder. For example, one
current theory hypothesizes that hopelessness (X) is a suf-
ficient cause of depression (Y) (Abramson et al., 1995,
1989). Or, more generally, if X occurs, then Y will also occur.
According to this theory, if you are hopeless enough about
your future, then you will become depressed. However, a
sufficient cause may not be a necessary cause. Continuing with the depression example, Abramson and colleagues
(1989) acknowledge that hopelessness is not a necessary
cause of depression; there are other causes of depression as
well.
Finally, what we study most often in psychopathol-
ogy research are contributory causes. A contributory cause is one that increases the probability of a disorder develop-
ing but is neither necessary nor sufficient for the disorder
to occur. More generally, if X occurs, then the probability of
Y occurring increases. For example, parental rejection
could increase the probability that a child will later have
difficulty in handling close personal relationships or could
increase the probability that being rejected in a relationship
in adulthood will precipitate depression. We say here that
parental rejection could be a contributory cause for the per-
son’s later difficulties, but it is neither necessary nor suffi-
cient (Abramson et al., 1989, 1995).
In addition to distinguishing among necessary, suffi-
cient, and contributory causes of abnormal behavior, we
must also consider the time frame under which the differ-
ent causes operate. Some causal factors occurring relatively
early in life may not show their effects for many years;
these would be considered distal risk factors (or distal causal
factors if the conditions described in Figure 3.1 are satis-
fied) that may contribute to a predisposition to develop a
disorder. For example, loss of a parent early in life, or hav-
ing abusive or neglectful parents as a child or adolescent,
may serve as a distal contributory cause predisposing a
person to depression or antisocial behaviors later in life. By
contrast, other factors operate shortly before the occur-
rence of the symptoms of a disorder; these would be con-
sidered proximal risk factors. Sometimes a proximal factor
may be a condition that proves too much for a child or
adult and triggers the onset of a disorder. A crushing dis-
appointment at school or work or severe difficulties with a
school friend or a marital partner are examples of more
proximal factors that could lead to depression. In other
cases, proximal factors might involve biological changes
such as damage to certain parts of the left hemisphere of
the brain, which can lead to depression.
A reinforcing contributory cause is a condition that tends
to maintain maladaptive behavior that is already occur-
ring. An example is the extra attention, sympathy, and
relief from unwanted responsibility that may come when a
person is ill; these pleasant experiences may unintention-
ally discourage recovery. Another example occurs when a
depressed person’s behavior alienates friends and family,
leading to a greater sense of rejection that reinforces the
existing depression (Joiner & Timmons, 2009).
feedback and bidirectionality in abnormal behaviour
Traditionally in the sciences, the task of determining cause-
and-effect relationships has focused on isolating the condi-
tion X (cause) that can be demonstrated to lead to condition
Y (effect). For example, when the alcohol content of the
blood reaches a certain level, alcoholic intoxication occurs.
When more than one causal factor is involved, as is often
the case, the term causal pattern is used. Here, conditions A,
B, C, and so on, lead to condition Y. In either case, this con-
cept of cause follows a simple linear model in which a given
variable or set of variables leads to a result either immedi-
ately or later. However, in the behavioral sciences, we deal
with a multitude of interacting causes, and often have dif-
ficulty distinguishing between what is a cause and what is
an effect. This occurs because effects can serve as feedback
that can in turn influence the causes. In other words, the
effects of feedback and the existence of mutual, two-way
(bidirectional) influences must be taken into account.
diathesis- stress models
Scientists try to understand how variables work together to
cause outcomes of interest by using conceptual models that
distinguish between different types of causal factors. Many
mental disorders are believed to develop when someone
who has a preexisting vulnerability for that disorder
experiences a major stressor. Models describing this kind of
situation are commonly known as diathesis–stress models
of abnormal behavior (e.g., Ingram & Luxton, 2005; Meehl,
1962; Monroe & Simons, 1991).A vulnerability, or diathesis,
is a predisposition toward developing a disorder that can
derive from biological, psychological, or sociocultural
causal factors. Stress, the response or experience of an
individual to demands that he or she perceives as taxing or
exceeding his or her personal resources, will be the focus of
Chapter 5. Stress often occurs when an individual
experiences chronic or episodic events that are undesirable
and lead to behavioral, physiological, and cognitive
accommodations (Schneiderman et al., 2005).
To translate these terms into the types of causal factors
described earlier, the diathesis results from one or more
relatively distal necessary or contributory causes, but is
generally not sufficient to cause the disorder. Instead, there
must be amoreproximal factor (the stressor), which may also
be contributory or necessary but is generally not sufficient by
itself to cause the disorder except in someone with the
diathesis. It is important to note that factors contributing to
the development of a diathesis are themselves sometimes
highly potent stressors, as whena child experiencesthe death
of a parent and may thereby acquire a predisposition or
diathesis for becoming depressed later in life.
Researchers have proposed several different ways in
which a diathesis and stress may combine to produce a disorder (Ingram & Luxton, 2005). In what is called the
additive model, the diathesis and the stress simply add up,
or sum together. Thus, a person with no diathesis or a
very low level of diathesis could still develop a disorder
when faced with high levels of stress, whereas a person
with a high level of a diathesis may need only a small
amount of stress before a disorder develops. In what is
called an interactive model, some amount of diathesis must
be present before stress will have any effect. Statistically
speaking, this is referred to as an interaction between the
two variables in which the effect between one variable
(e.g., stress) and the outcome (e.g., disorder) varies at dif-
ferent levels of the third variable (e.g., diathesis). For
instance, in this case, stress might have no association
with the likelihood of developing a disorder in the absence
of a diathesis (e.g., no genetic predisposition to depres-
sion), whereas for someone with the diathesis, the likeli-
hood of developing the disorder might go up with
increasing levels of stress. More complex models also are
possible because diatheses often exist on a continuum,
ranging from zero to high levels. Each of these possibili-
ties is illustrated in Figure 3.2.
In contrast to risk factors that increase the likelihood
of negative outcomes, protective factors decrease the like-
lihood of negative outcomes among those at risk (Kraemer
et al., 1997). Note that a protective factor is not simply the
absence of a risk factor, but instead is something that
actively buffers against the likelihood of a negative out-
come among those with some risk factor(s). One impor-
tant protective factor in childhood is having a family
environment in which at least one parent is warm and
supportive, allowing the development of a good attach-
ment relationship between the child and parent that can
protect against the harmful effects of an abusive parent
(Masten & Coatsworth, 1998).
Protective factors are not necessarily positive experi-
ences. Indeed, sometimes exposure to stressful experi-
ences that are dealt with successfully can promote a sense
of self-confidence or self-esteem and thereby serve as a
protective factor. Thus, some stressors paradoxically pro-
mote coping. This “steeling” or “inoculation” effect is
more likely to occur with moderate stressors than with
mild or extreme stressors (Barlow, 2002; Hetherington,
1991; Rutter, 1987). Some protective factors have nothing
to do with experiences at all but are simply some quality
or attribute of a person. For example, adolescents who
score high on emotional intelligence are less likely to show
negative outcomes following childhood abuse (Cha &
Nock, 2009).
Protective factors most often, but not always, lead to
resilience—the ability to adapt successfully to even very
difficult circumstances. An example is the child who perse-
veres and does well in school despite his or her parent’s drug addiction or physical abuse. More generally, the term
resilience has been used to describe the phenomenon that
“some individuals have a relatively good outcome despite
suffering risk experiences that would be expected to bring
about serious sequelae” (Rutter, 2007, p. 205). A more
everyday way of thinking of resilience is in terms of “over-
coming the odds” against you. There is increasing evidence
that if a child’s fundamental systems of adaptation (such as
intelligence and cognitive development, ability to self-
regulate, motivation to achieve mastery, effective parent-
ing, and well-functioning neurobiological systems for
handling stress) are operating normally, then most threat-
ening circumstances will have minimal impact on him or her (Masten, 2001; Sapienza & Masten, 2011). Problems
tend to arise when one or more of these systems of adap-
tation is weak to begin with (e.g., low intelligence or
poorly functioning neurobiological systems for handling
stress; Lester et al., 2006) or when a serious stressor dam-
ages one or more of these systems (e.g., when a parent
dies). Problems can also arise when the level of challenge
far exceeds human capacity to adapt (e.g., exposure to
chronic trauma in war or chronic maltreatment in abusive
families; Ungar, 2015). We should also note, however, that
resilience should not be thought of as an all-or-none
capacity, and some research suggests that resilient chil-
dren (that is, those who show high social competence
despite high stress) may also experience considerable
self-reported emotional distress. Moreover, children who
show resilience in one domain may show significant dif-
ficulties in other domains.
In sum, we can distinguish between causes of abnor-
mal behavior that lie within and are part of the biological
makeup or prior experience of a person—diatheses, vul-
nerabilities, or predispositions—and causes that pertain to
current challenges in a person’s life—stressors. Typically,
neither the diathesis nor the stress is by itself sufficient to cause the disorder, but in combination they can sometimes
lead the individual to behave abnormally. In addition, we
can examine protective factors, which may derive either
from particular types of experiences or from certain quali-
ties of the person, that can promote resilience in the face of
vulnerability and stress.
biological perspectives to undertsnadng the causes of abnormal behaviour
As we saw in the discussion of general paresis and its
link to syphilis in Chapter 2, the traditional biological
viewpoint focuses on mental disorders as diseases, many
of the primary symptoms of which are cognitive, emo-
tional, or behavioral. Mental disorders are thus viewed
as disorders of the central nervous system, the auto-
nomic nervous system, and/or the endocrine system that
are either inherited or caused by some pathological pro-
cess. At one time, people who adopted this viewpoint
hoped to find simple biological explanations. Today,
however, most people recognize that such explanations
are rarely simple, and many also acknowledge that psy-
chological and sociocultural causal factors play impor-
tant roles as well.
The disorders first recognized as having biological or
organic components were those associated with gross
destruction of brain tissue. These disorders are neurologi-
cal diseases—that is, they result from the disruption of
brain functioning by physical or biochemical means and
often involve psychological or behavioral aberrations. For
example, damage to certain areas in the brain can cause
memory loss, and damage to the left hemisphere that
occurs during a stroke can cause depression.
However, most mental disorders are not caused by
neurological damage per se. For example, abnormalities in
neurotransmitter systems in the brain can lead to mental
disorders without causing damage to the brain. Moreover,
the bizarre content of delusions and other abnormal men-
tal states like hallucinations can never be caused simply
and directly by brain damage. Consider the example of a
person with schizophrenia or general paresis who claims
to be Napoleon. The content of such delusions must be the
by-product of some sort of functional integration of differ-
ent neural structures, some of which have been “pro-
grammed” by personality and learning based on past
experience (e.g., having learned who Napoleon was).
We focus here on four categories of biological factors
that seem particularly relevant to the development of mal-
adaptive behavior: (1) genetic vulnerabilities, (2) brain
dysfunction and neural plasticity, (3) neurotransmitter and
hormonal abnormalities in the brain or other parts of the
central nervous system, and (4) temperament. Each of
these categories encompasses a number of conditions that
influence the quality and functioning of our bodies
and our behavior. They are often not independent of each
other but rather interact with one another. Moreover,
different factors may play more or less important roles in
different people.
biological - genetic vulnerabilities
Genes are very long molecules of DNA (deoxyribonucleic
acid) that are present at various locations on chromosomes.
Chromosomes are the chain-like structures within a cell
nucleus that contain the genes. Genes are the carriers of the
information that we inherit from our parents (individuals
have two copies of each gene—one from each of our par-
ents), and each gene exists in two or more alternate forms
called alleles. Genes don’t fully determine whether a person
develops a mental disorder; however, there is substantial
evidence that most mental disorders show at least some
genetic influence (Plomin et al., 2013; Rutter, 2006a). Some
of these genetic influences, such as broad temperamental
features, are first apparent in newborns and children. For
example, some children are just naturally more shy or anx-
ious, whereas others are more outgoing (Fox et al., 2010;
Kagan & Fox, 2006). However, some genetic sources of vul-
nerability do not manifest themselves until adolescence or
adulthood, when most mental disorders appear for the
first time.
Each human cell has 23 pairs of chromosomes
(46 total) containing genetic materials that encode the
hereditary plan for each individual. One copy of each chro-
mosome comes from the mother and one from the father.
Twenty-two of these chromosome pairs determine, by their
biochemical action, an individual’s general anatomical and
other physiological characteristics. The remaining pair, the
sex chromosomes, determines the individual’s sex. If both of these are X chromosomes, the offspring is a female (XX). If
the sex chromosome inherited from the father is a Y chro-
mosome, the offspring is a male (XY). (See Figure 3.3.)
Research in developmental genetics has shown that
abnormalities in the structure or number of chromosomes
can be associated with major defects or disorders. For exam-
ple, Down syndrome is a type of intellectual disability in
which there is a trisomy (a set of three chromosomes instead
of two) in chromosome 21 (see Chapter 15). Here the extra
chromosome is theprimary cause of the disorder. Anomalies
may also occur in the sex chromosomes, producing a variety
of complications, such as ambiguous sexual characteristics,
that may predispose apersontodevelop abnormal behavior.
More typically, however, personality traits and mental
disordersare not affectedby chromosomalabnormalities per
se. Instead they are more often influenced either by abnor-
malities in some of the genes on the chromosomes or by nat-
urally occurringvariations of genesknown as polymorphisms.
Although you will often hear about discoveries that “the
gene” for a particular disorder has been discovered, vulner-
abilities to mental disorders are almost always polygenic,
which means they are influenced by multiple genes or by
multiple polymorphisms of genes,with any one genehaving
only very small effects (Kendler, 2005; Plomin et al., 2013). In
other words, a genetically vulnerable person has usually
inherited a large number of genes, or polymorphisms of
genes, that operate together in an additive or interactive
fashion to increase vulnerability. Collectively these genes
may lead to structural abnormalities in the central nervous system, to abnormalities in the regulation of brain chemistry
and hormonal balance, or to excesses or deficiencies in the
reactivity of the autonomic nervous system, which is
involved in mediating many of our emotional responses.
In the field of abnormal psychology, genetic influences
rarely express themselves in a simple and straightforward
manner. This is because behavior, unlikesome physical char-
acteristics such as eye color, is not determined exclusively by
genetic endowment; it isa product of the organism’s interac-
tion with the environment. In other words, genes can affect
behavior only indirectly. Gene “expression” is normally not
a simple outcome of the information encoded in DNAbut is,
rather, the end product of an intricate process that may be
influenced by the internal (e.g., intrauterine) and external
environment. Indeed, certain genes can actually be “turned
on,” or activated, and “turned off,” or deactivated, in
response to environmental influences such as stress.
A person’s total genetic endowment is referred to as
her or his genotype and, except for identical twins, no two
humans have the same genetic makeup. The observed
structural and functional characteristics that result from an
interaction of the genotype and the environment are
referred to as a person’s phenotype.
GENOTYPE–ENVIRONMENT INTERACTIONS In most
cases, genetic factors are not necessary and sufficient to
cause mental disorders but instead can contribute to a vul-
nerability or diathesis to develop psychopathology that
only happens if there is a significant stressor in the person’s
life (as in the diathesis–stress models described earlier).
This is known as a genotype–environment interaction.
GENOTYPE–ENVIRONMENT CORRELATIONS In many
cases, there is evidence that genes can actually shape the
environmental experiences a child has, thus affecting the
phenotype in important ways. For example, a child who is
genetically predisposed to aggressive behavior may be
rejected by his or her peers in early grades because of the
aggressive behavior. Such rejection may lead the child to go
on to associate with similarly aggressive and delinquent
peers in later grades, leading to an increased likelihood of
developing a full-blown pattern of delinquency in adoles-
cence. When the genotype shapes theenvironmental experi-
encesa child has in this way, we refer to thisphenomenon as
a genotype–environment correlation (Plomin et al., 2013;
Rutter, 2006a, 2007). Researchers have found three impor-
tant ways in which an individual’s genotype may shape his
or her environment (Jang et al., 2005; Plomin et al., 2013).
The child’s genotype may have what has been termed
a passive effect on the environment, resulting from the
genetic similarity of parents and children.
- The child’s genotype may evoke particular kinds of re-
actions from the social andphysical environment—a so-
called evocative effect. - The child’s genotype may play a more active role in
shaping theenvironment—a so-called activeeffect. In this
case the child seeks out or builds an environment that is
congenial—a phenomenon known as “niche building.”
methods for studying genetic influences - behvaiiru genetics looking at the heritability of mental disorders. the family history method. the twin method - looking at concordance rates. the adoption method. these methods separated genetic and environmental influences so allow for testing of influence of enviornemtal factors.
biological - Brian dysfunction and neural plasticity
Specific brain lesions with observable defects in brain tis-
sue are rarely a primary cause of psychiatric disorders.
However, advances in understanding how more subtle
deficiencies of brain structure or function are implicated in
many mental disorders have been increasing at a rapid
pace in the past few decades. Some of these advances come
from the greater availability of sophisticated new neuroim-
aging techniques to study the function and structure of the
brain (see Chapter 4 for more details). Research has
revealed that genetic factors guide brain development—so
these different pieces of the biological puzzle are all related
(Hibar et al., 2015). However, we also know that genetic
programs for brain development are not so rigid and deter-
ministic as was once believed (Gottesman & Hanson, 2005;
Thompson & Nelson, 2001). Instead, there is considerable
neural plasticity—flexibility of the brain in making changes
in organization and function in response to pre- and post-
natal experiences, stress, diet, disease, drugs, maturation,
and so forth. Existing neural circuits can be modified, or
new neural circuits can be generated (Wamsley & Fishell,
2017). The effects can be either beneficial or detrimental to
the individual, depending on the circumstances.
Research on neural and behavioral plasticity, in combi-
nation with the work described earlier on genotype–
environment correlations, makes it clear why developmen-
tal psychopathologists have been devoting increasing
attention to a developmental systems approach (Masten,
2006; Spencer et al., 2009), which acknowledges that genet-
ics influences neural activity, which in turn influences
behavior, which in turn influences the environment, but
also that these influences are bidirectional.
biological - imbalances of neurotransmitters and hormones
Imbalances in neurotransmitters in the brain can result in abnormal behavior.
Psychological stress can bring on neurotransmitter imbalances.
Excessive production and release of neurotransmitters into the synapses can cause a functional excess in levels of that neurotransmitter.
Dysfunctions in the normal processes by which neurotransmitters are deactivated can result in imbalances.
Problems with the receptors in the postsynaptic neuron can also cause imbalances.
Different disorders are thought to stem from different patterns of neurotransmitter imbalances in various brain areas.
Medications used to treat various disorders are often believed to operate by correcting these imbalances.
The widely prescribed antidepressants Prozac and Zoloft are designed to slow the reuptake of the neurotransmitter serotonin.
Five different kinds of neurotransmitters have been most extensively studied in relationship to psychopathology.
The first three neurotransmitters belong to a class called monoamines.
Norepinephrine has been implicated as playing an important role in emergency reactions and basic motives.
Norepinephrine also plays a role in attention and orientation.
Glutamate and GABA are also neurotransmitters studied in relationship to psychopathology.
Over a hundred neurotransmitters have been discovered to date.
Neurons that are sensitive to a particular neurotransmitter tend to cluster together, forming neural paths between different parts of the brain known as chemical circuits.- Dopamine is involved in pleasure, cognitive processing, schizophrenia, and addictive disorders.
Serotonin is another neurotransmitter.
Nerve impulses travel from the cell body or dendrites of one neuron down the axon.
Neurotransmitter substances are released into the synapse, which is a tiny fluid-filled space between the axon endings of one neuron and the dendrites or cell body of another neuron.
Neurotransmitters are chemical substances that are released into the synapse by the presynaptic neuron when a nerve impulse occurs.
The neurotransmitter substances act on the postsynaptic membrane of the dendrite (or cell body) of the receiving neuron, which has specialized receptor sites where the neurotransmitter substances pass on their message.
Neurotransmitters can stimulate the postsynaptic neuron to either initiate an impulse or inhibit impulse transmission.
Neurotransmitter substance does not stay around indefinitely and is quickly destroyed by an enzyme or returned to storage vesicles in the axon endings by a reuptake mechanism.
Monoamine oxidase is an enzyme that can destroy excess neurotransmitters in the presynaptic terminal.
There are many different kinds of neurotransmitters that can increase or inhibit the likelihood of the postsynaptic neuron firing.
The concentration of certain neurotransmitters within the synapse affects whether the neural message is successfully transmitted to the postsynaptic neuron.
Synapse, axon, neurotransmitter, enzyme, receptor, dendrite, and mitochondria are all terms related to interneuronal transmission.
Neurotransmitters can stimulate the postsynaptic neuron to either initiate an impulse or inhibit impulse transmission.
Reuptake is a process of reabsorption by which the neurotransmitters are reabsorbed
Epinephrine (adrenaline) and cortisol are stress hormones produced by the adrenal gland.
Cortisol provides negative feedback to the hypothalamus and pituitary to decrease the release of CRH and ACTH.
Malfunctioning of the negative feedback system has been implicated in various forms of psychopathology such as depression and posttraumatic stress disorder.
Imbalance in sex hormones, such as male hormones, can contribute to maladaptive behavior.
Gonadal hormonal influences on the developing nervous system also contribute to some differences between behavior in men and women.
Neurotransmitter serotonin plays an important role in emotional disorders such as anxiety and depression.
Excitatory neurotransmitter glutamate has been implicated in schizophrenia.
Neurotransmitter GABA is strongly implicated in reducing anxiety and other emotional states characterized by high levels of arousal.
Many forms of psychopathology have been associated with various abnormalities in neurotransmitter functioning and altered sensitivities of receptor sites.
Medications used to treat various disorders act at the synapse as their site of action.
Certain medications act to increase or decrease the concentrations of pertinent neurotransmitters in the synaptic gap.
Medications may block the reuptake process, alter the sensitivity of receptor sites, or affect the actions of enzymes that break down neurotransmitter substances.
The synapse is an important site of action for many medications used to treat psychopathology.
Each neurotransmitter will be discussed at greater length when relevant disorders are discussed in later chapters.- Medications that enhance the effects of a neurotransmitter on the post-synaptic neuron are called agonists, while those that inhibit the effects of a neurotransmitter on a post-synaptic neuron are called antagonists.
Hormones are chemical messengers produced and released by endocrine glands that affect target cells in various parts of the brain and body.
The hypothalamus regulates the pituitary gland, which is the master gland of the body that produces hormones that regulate other endocrine glands.
The hypothalamic-pituitary-adrenal (HPA) axis is an important set of interactions that involves messages in the form of corticotropin-releasing hormone (CRH) traveling from the hypothalamus to the pituitary, which then releases adrenocorticotropic hormone (ACTH) that stimulates the cortical part of the adrenal gland.
The HPA axis is involved in regulating the body’s stress response by releasing epinephrine and cortisol.
Hormonal imbalances have been linked to some forms of psychopathology.
Hormones influence diverse events such as fight-or-flight reactions, sexual responses, physical growth, and many other physical expressions of mental states.
The neuroendocrine system links the central nervous system to the endocrine system.
The pituitary gland produces a variety of hormones that regulate or control other endocrine glands in the body.
The hypothalamus periodically sends hormone signals to the pituitary gland.
The adrenal gland is located on top of the kidneys and produces epinephrine and cortisol.
The HPA axis involves the hypothalamus, pituitary gland, and adrenal gland.
Corticotropin-releasing hormone (CR
biological - temperament
Positive affect and activity level are related to the adult dimension of extraversion.
Attentional persistence and effortful control are related to the adult dimension of constraint or control.
Boys show slightly higher levels of activity and intense pleasure than girls, whereas girls have greater control of their impulses and greater ability to regulate their attention.
Temperament shows a moderate degree of stability from late in the first year of life through at least middle childhood, although it can change.
The temperament of an infant or young child has profound effects on a variety of important developmental processes.
Children with a fearful temperament have many opportunities for the classical conditioning of fear to situations in which fear is provoked.
Children with high levels of positive affect and activity are more likely to show high levels of mastery motivation.
Children with high levels of fear and sadness are less likely to show mastery motivation.
Children with high levels of negative emotionality are more difficult for parents to be supportive of, and different parents have different styles of parenting such children.
Families with lower socioeconomic status are, on average, less supportive of difficult children than families of mid to high socioeconomic status.
Temperament may set the stage for the development of various forms of psychopathology later in life.
Children who are fearful and hypervigilant in many novel or unfamiliar situations have been labeled behaviorally inhibited by Kagan, Fox, and their colleagues.
Behaviorally inhibited trait has a significant heritable component, and it is a risk factor for the development of anxiety disorders later in childhood and probably in adulthood.- Temperament refers to a child’s reactivity and characteristic ways of self-regulation, which is believed to be biologically programmed.
Babies show differences in their characteristic emotional and arousal responses to various stimuli and in their tendency to approach, withdraw, or attend to various situations.
Some babies are naturally sensitive to slight sounds or sunlight, while others seem insensitive to such stimulation.
Genetic factors strongly influence the temperament of babies, but prenatal and postnatal environmental factors also play a role in their development.
Early temperament is thought to be the basis from which our personality develops.
Approximately five dimensions of temperament can be identified in babies starting at about 2 to 3 months of age: fearfulness, irritability/frustration, positive affect, activity level, and attentional persistence/effortful control.
These dimensions of temperament seem to be related to the three important dimensions of adult personality: neuroticism or negative emotionality, extraversion or positive emotionality, and constraint.
The infant dimensions of fearfulness and irritability correspond to the adult dimension of neuroticism.
Temperament is consistent over time, causing us to have similar reactions in similar contexts.
Highly uninhibited 2-year-old children may have difficulty learning moral standards for their behavior from parents or society, and they have been shown at age 13 to exhibit more aggressive and delinquent behavior.
Temperament is strongly influenced by genetic factors, but prenatal and postnatal environmental factors also play a role in their development.
Rothbart, Derryberry, and Hershey (2000) conducted research on temperament and identified five dimensions of temperament in babies.
The five dimensions of temperament identified by Rothbart, Derryberry, and Hers
psychological perspective - psychodynamic perspective
Sigmund Freud founded the
psychoanalytic school, which emphasized the role of uncon-
scious motives and thoughts and their dynamic interrela-
tionships in the determination of both normal and
abnormal behavior. A key concept here is the unconscious.
According to Freud, the conscious part of the mind repre-
sents a relatively small area, whereas the unconscious part,
like the submerged part of an iceberg, is the much larger
portion. In the depths of the unconscious are the hurtful
memories, forbidden desires, and other experiences that
have been repressed—that is, pushed out of consciousness.
However, Freud believed that unconscious material con-
tinues to seek expression and emerges in fantasies, dreams,
slips of the tongue, and so forth. Until such unconscious material is brought to awareness and integrated into the
conscious part of the mind—for example, through psycho-
analysis (a form of psychotherapy Freud developed; see
Chapter 16)—it may lead to irrational and maladaptive
behavior. For our purposes, a general overview of the prin-
ciples of classical psychoanalytic theory will suffice. We
then discuss several of the newer psychodynamic perspec-
tives, which were the second generation of theories that
stemmed in some important ways out of Freud’s original
psychoanalytic theory and yet also departed from it in sig-
nificant ways.
FUNDAMENTALS OF FREUD’S PSYCHOANALYTIC
THEORY In an effort to explain human behavior, Freud
theorized that a person’s behavior results from the interac-
tion of three key components of the personality that he
called the id, ego, and superego.
The superego is the outgrowth of internalizing the taboos and moral values of society concerning what is right and wrong, essentially what we refer to as the conscience.
The superego becomes an inner control system that deals with the uninhibited desires of the id.
The interplay of id, ego, and superego is of crucial significance in determining behavior.
Anxiety plays a key causal role in most forms of psychopathology, according to Freud’s psychoanalytic viewpoint.
Anxiety is the body’s natural warning system that signals impending danger and the need to take corrective action.
Anxiety is sometimes overtly experienced and at other times it is repressed and then transformed into and manifested in other overt symptoms such as conversion blindness or paralysis.
When material is brought to awareness and integrated into the conscious part of the mind, it may lead to irrational and maladaptive behavior.
Classical psychoanalytic theory suggests that a person’s behavior results from the interaction of three key components of the personality: the id, ego, and superego.
The id is the source of instinctual drives and is the first structure to appear in infancy.
Inner mental conflicts arise because the three subsystems (id, ego, and superego) are striving for different goals.
Unresolved intrapsychic conflicts lead to mental disorder.
Freud developed psychoanalysis, a form of psychotherapy that brings material to awareness and integrates it into the conscious part of the mind.
Several newer psychodynamic perspectives stem from Freud’s original psychoanalytic theory but also depart from it in significant ways.
The principles of classical psychoanalytic theory provide a general overview of Freud’s explanation of human behavior.- Freud believed that drives could be divided into two opposing types: life instincts and death instincts.
Life instincts are constructive drives primarily of a sexual nature and constitute the libido.
Death instincts are destructive drives that tend towards aggression, destruction, and eventual death.
The id operates on the pleasure principle and is concerned only with the immediate gratification of instinctual needs.
The ego mediates between the demands of the id and the realities of the external world and assumes the role of mediating between the physical needs of the body/id and the need to find an appropriate place and time.
One of the basic functions of the ego is to meet id demands but in such a way as to ensure the well-being and survival of the individual.
The ego’s adaptive measures are referred to as secondary process thinking, and the ego operates on the reality principle.
According to Freud, id demands, especially sexual and aggressive strivings, are inherently in conflict with the rules and prohibitions imposed by society.
The ego requires the use of reason and other intellectual resources in dealing with the external world, as well as the exercise of control over id demands.
The id can generate mental images and wish-fulfilling fantasies, referred to as primary process thinking, but it cannot undertake the realistic actions needed to meet instinctual demands.
Freud used the term sexual in a broad sense to refer to almost anything pleasurable, from eating to painting.
Anxiety is almost universally experienced at some point.
The woman in the image shows her anxiety while awaiting news about the outcome of surgery on her sick child.
Freud believed that the basic emotional and psychic energy of life was the libido.
The pleasure principle is the id’s tendency to seek
There are five stages of psychosexual development that individuals pass through from infancy through puberty.
The oral stage occurs during the first two years of life and is characterized by the mouth being the principal erogenous zone.
The anal stage occurs from ages 2 to 3, and the anus provides the major source of pleasurable stimulation during toilet training.
The phallic stage occurs from ages 3 to 5 or 6, and self-manipulation of the genitals provides the major source of pleasure.
During the latency period, from ages 6 to 12, sexual motivations decrease in importance as a child becomes preoccupied with developing skills and other activities.
The deepest feelings of pleasure come from sexual relations after puberty, which is known as the genital stage.
Appropriate gratification during each stage is important if a person is to avoid being fixated at that level.
Freud believed that an individual who does not receive adequate oral gratification may be prone to excessive eating or other forms of oral stimulation in adulthood.
Anxiety is a normal response to danger or threat, but when it is excessive and persistent, it can be considered problematic or pathological.
The ego can cope with elevated anxiety through rational measures, but when anxiety exists only in the unconscious, it cannot be dealt with through rational measures.
Ego-defense mechanisms are irrational protective measures that help reduce anxiety by pushing painful ideas out of consciousness.
Freud proposed that defense mechanisms reduce anxiety by not dealing directly with the problem.
Forgetting a dental appointment is an example of a defense mechanism.
There are several types of ego-defense mechanisms, which are described in Table 3.1.
Ego-defense mechanisms help individuals cope with anxiety and protect their- Freud proposed that there are five psychosexual stages of development.
The demands of the id are evident in early childhood.
Babies pass through an oral stage, in which sucking is a dominant pleasure.
Ego-defense mechanisms are used to prevent painful or dangerous thoughts from entering consciousness.
Displacement is an ego-defense mechanism that involves discharging pent-up feelings on objects less dangerous than those arousing the feelings.
Fixation is an ego-defense mechanism that involves attaching oneself in an unreasonable or exaggerated way to some person, or arresting emotional development on a childhood or adolescent level.
Projection is an ego-defense mechanism that involves attributing one’s unacceptable motives or characteristics to others.
Rationalization is an ego-defense mechanism that involves using contrived explanations to conceal or disguise unworthy motives for one’s behavior.
Reaction formation is an ego-defense mechanism that involves preventing the awareness or expression of unacceptable desires by an exaggerated adoption of seemingly opposite behavior.
Regression is an ego-defense mechanism that involves retreating to an earlier developmental level involving less mature behavior and responsibility.
Repression is an ego-defense mechanism that involves preventing painful or dangerous thoughts from entering consciousness.
Sublimation is an ego-defense mechanism that involves channeling frustrated sexual energy into substitutive activities.
The DSM-IV-TR is a source used for this information.
An example of displacement is a woman harassed by her boss at work initiating an argument with her husband.
An example of fixation is an unmarried, middle-aged man still depending on his mother to provide his basic needs.
An example of projection is an expansionist-minded dictator of a totalitarian state being convinced that neighboring countries are planning to invade.
psychological perspective - behavioural perspective
The process of classical conditioning was discovered by Russian physiologist Ivan Pavlov.
Dogs gradually began to salivate in response to a nonfood stimulus such as a bell after the stimulus had been regularly accompanied by food.
Food is the unconditioned stimulus, and salivation is the unconditioned response.
A stimulus that signals food delivery and eventually elicits salivation is called a conditioned stimulus (CS).
Conditioning has occurred when the presentation of the conditioned stimulus alone elicits salivation—the conditioned response (CR).
Classical conditioning is not as blind or automatic as was once thought, and animals actively acquire information about what CSs allow them to predict, expect, or prepare for an upcoming biologically significant event (the UCS).
Behavioral psychologists believed that the study of subjective experience did not provide acceptable scientific data because such observations were not open to verification by other investigators.
Only the study of directly observable behavior and of the stimuli and reinforcing conditions that control it could serve as a basis for understanding human behavior.
The hallmark of classical conditioning is that a formerly neutral stimulus—the CS—acquires the capacity to elicit biologically adaptive responses through repeated pairings with the UCS.
Conditioning also occurs when a neutral CS is paired with a painful or frightening stimulus such as a mild electric shock or loud noise, and fear rather than salivation is conditioned.
The conditioned reflex was discovered by Ivan Pavlov.
The behavioral perspective arose in the early twentieth century in part as a reaction against the unscientific methods of psychoanalysis.
Behavioral psychologists believed that the study of directly observable behavior is the only basis for understanding human behavior.
Classical conditioning is a process where a neutral stimulus becomes a conditioned stimulus that elicits a conditioned response- The behavioral approach views learning as the modification of behavior due to experiences.
The behaviorists focus on the effects of environmental conditions or stimuli on the acquisition, modification, and elimination of different types of response patterns.
Classical conditioning is a type of learning where a neutral stimulus is paired repeatedly with an unconditioned stimulus that naturally elicits an unconditioned behavior.
The behavioral view of abnormal behavior and its treatment are tied to experimental work on classical conditioning.
Watson was a behaviorist who believed that conditioning could train any healthy child to become any sort of adult one wished, and that abnormal behavior could be modified through reconditioning.
Behaviorally oriented psychologists still accept many of the basic tenets of Watson’s doctrine today, although they are more cautious in their claims.
Operant conditioning is a type of conditioning where the consequences of behavior influence behavior, and an individual learns how to achieve a desired goal.
In operant conditioning, the concept of reinforcement is essential, which refers either to the delivery of a reward or pleasant stimulus, or to the removal of or escape from an aversive stimulus.
New responses are learned and tend to recur if they are reinforced, and an instrumental response appears to be especially persistent when reinforcement is intermittent.
Initially a high rate of reinforcement may be necessary to establish an instrumental response, but lesser rates are usually sufficient to maintain it.
In instrumental conditioning, it is now believed that the animal or person learns a response–outcome expectancy, that is, learns that a response will lead to a reward outcome.
Classical conditioning is the type of conditioning studied by Pavlov and Watson.
In classical conditioning, a stimulus that is initially neutral (the conditioned stimulus or CS) becomes associated with a stimulus that elicits a reflexive response (the unconditioned stimulus or UCS).
New responses are learned in operant conditioning, whereas classical conditioning involves the pairing of stimuli.
Classically conditioned responses are well maintained over time and are not simply forgotten.
Only CSs that provide reliable and nonredundant information about the occurrence of a UCS acquire the capacity to elicit CRs.
Conditioning will not occur if UCSs- If a conditioned stimulus (CS) is presented repeatedly without the unconditioned stimulus (UCS), the conditioned response (CR) gradually extinguishes.
However, extinction should not be confused with unlearning because the response may return at some future point in time, which is known as spontaneous recovery.
A weaker CR may still be elicited in different environmental contexts than in the one where the extinction process took place.
Any extinction of fear that has taken place in a therapist’s office may not necessarily generalize completely and automatically to other contexts outside the therapist’s office.
Classical conditioning can condition many physiological and emotional responses, including fear, anxiety, sexual arousal, and drug addiction.
Pavlov’s discoveries in classical conditioning excited John B. Watson, who changed the focus of psychology to the study of overt behavior rather than the study of theoretical mentalistic constructs, an approach he called behaviorism.
Reinforcement is key in operant conditioning to achieve a desired goal with either the delivery of a reward or the removal of an aversive stimulus.
psychological perspective - cognitive - behavioural perspective
Since the 1950s many psychologists, including some learn-
ing theorists, focused on cognitive processes and their
impact on behavior. Cognitive psychology involves the study of basic information-processing mechanisms such as
attention and memory, as well as higher mental processes
such as thinking, planning, and decision making. The
current emphasis within psychology as a whole on under-
standing all of these facets of normal human cognition
originally began as a reaction against the relatively mecha-
nistic nature of the traditional, radical behavioral view-
point (espoused by Watson and Skinner), including its
failure to attend to the importance of mental processes—
both in their own right and for their influence on emotions
and behavior.
bandura - stressed that human
beings regulate behavior by internal symbolic processes.
That is, we learn by internal reinforcement. According to
Bandura, we prepare ourselves for difficult tasks, for exam-
ple, by visualizing what the consequences would be if we
did not perform them.
schemas and cognitive distortions - about ourselves, other people , the world around us, schemas about social roles
Our self-schemas include our views on
who we are, what we might become, and what is important
to us. However, schemas are also sources of psychological vul-
nerabilities because some of our schemas or certain aspects
of our self-schemas may be distorted and inaccurate. addition, we often hold some schemas—even distorted
ones—with conviction, making them resistant to change.
ATTRIBUTIONS, ATTRIBUTIONAL STYLE, AND
PSYCHOPATHOLOGY Attribution theory has also con-
tributed significantly to the cognitive-behavioral approach
(Gotlib & Abramson, 1999). Attribution is simply the pro-
cess of assigning causes to things that happen. We may
attribute behavior to external events such as rewards or
punishments (“He did it for the money”), or we may
assume that the causes are internal and derive from traits
within ourselves or others (“He did it because he is so gen-
erous”). Causal attributions help us explain our own or
other people’s behaviors and make it possible to predict
what we or others are likely to do in the future. A student
who fails a test may attribute the failure to a lack of intelli-
gence (a personal trait) or to ambiguous test questions or
unclear directions (environmental causes).
COGNITIVE THERAPY Beck, who is generally consid-
ered thefounder of cognitive therapy, has been enormously
influential in the development of cognitive-behavioral
treatment approaches to various forms of psychopathol-
ogy.
social perspective - early deprivation or trauma
Children who do not have the resources that are typically
supplied by parents or parental surrogates may be left with
deep and sometimes irreversible psychological scars.
These needed resources range from food and shelter to
love and attention. Deprivation of such resources can occur
in several forms. The most severe manifestations of depri-
vation are usually seen among abandoned or orphaned children, who may be either institutionalized or placed in a
succession of unwholesome and inadequate foster homes.
However, it can also occur in intact families where, for one
reason or another, parents are unable (for instance, because
of mental disorder) or unwilling to provide close and fre-
quent human attention and nurturing.
institutionalisation means children receive less warmth and physical contact, less intellectual, emotional, and social
stimulation; and a lack of encouragement and help in posi-
tive learning. Many children
institutionalizedininfancy andearly childhood show severe
emotional, behavioral, and learning problemsand are atrisk
for disturbed attachment relationships and psychopathol-
ogy (Bos et al., 2011; Ellis et al., 2004; Smyke et al., 2007).
neglect and abuse in the home - Outright parental abuse (physical or sexual or both) of
children has been associated with many negative effects
on children’s emotional, intellectual, and physical devel-
opment, although some studies have suggested that, at
least among infants, gross neglect may be worse than hav-
ing an abusive relationship. Abused children often have a
tendency to be overly aggressive (both verbally and physi-
cally), even to the extent of bullying. Some even respond
with anger and aggression to friendly overtures from
peers (Cicchetti & Toth, 2005).
separation - Bowlby (1960, 1973) first summarized the
traumatic effects, for children from 2 to 5 years old, of being
separated from their parents during prolonged periods of
hospitalization.
social - problems in parenting style
Even in the absence of severe deprivation, neglect, or
trauma, many kinds of deviations in parenting can have
profound effects on a child’s subsequent ability to cope
with life’s challenges and thus can create a child’s vulner-
ability to various forms of psychopathology. Therefore,
although their explanations vary considerably, the psycho-
logical viewpoints on causes of psychopathology all focus
on the behavioral tendencies a child acquires in the course
of early social interaction with others—chiefly parents or
parental surrogates (Parke, 2004; Sroufe et al., 2000).
parenting style diagram in photos
social - marital discord and divorce
Disturbed parent–child patterns such as parental rejection
are rarely found in severe form unless the total familial
context is also abnormal. Thus, disturbed family structure
is an overarching risk factor that increases an individual’s
vulnerability to particular stressors. We will distinguish
between intact families where there is significant marital
discord and families that have been disrupted by divorce
or separation.
MARITAL DISCORD All couples argue, but when taken
to an extreme, marital discord can have damaging psycho-
logicaleffectson both adultsand theirchildren (e.g.,Amato,
2006; Amato & Booth, 2001; Parke, 2004). More severe cases
of marital discord may expose children to one or more of
the stressors we have already discussed: child abuse or
neglect, the effects of living with a parent with a serious
mental disorder, authoritarian or neglectful/uninvolved
parenting, and spouse abuse. But even less severe cases of
marital discord also have negative effects on many chil-
dren.
divorced - Effects of Divorce on Parents Unhappy marriages are dif-
ficult, but ending a marital relationship can also be enor-
mously stressful for the adults, both mentally and
physically. The negative effects are often temporary, with
most people being able to adapt constructively within 2 to
3 years, but some adults never fully recover (Amato, 2000;
Hetherington, 2003a). Divorced and separated persons are
overrepresented among psychiatric patients, although the
direction of the causal relationship is not always clear. It
should also be recognized, however, that divorce actually
benefits some individuals (Amato, 2000, 2010)—with some
evidence that women are more likely to benefit than men
(Hetherington, 2003a). Effects of Divorce on Children Divorce can have traumatic
effects on children, too. Feelings of insecurity and rejection
may be aggravated by conflicting loyalties. Delinquency
and a wide range of other psychological problems such as
anxiety and depression are much more frequent among
children and adolescents from divorced families than
among those from intact families, although it is likely that
a contributing factor here is prior or continuing parental
strife (Strohschein, 2005). However, findings also show
that, on average, such children had shown these problems
to some degree even before their parents divorced (Amato,
2010; Strohschein, 2005).
social - low socioeconomic status and unemployment
In our society, the lower the socioeconomic class, the higher
the incidence of mental disorders (World Health Organiza-
tion, 2014). The strength of this inverse correlation varies
with different types of mental disorder, however. For exam-
ple, antisocial personality disorder is strongly related to
socioeconomic status (SES), occurring about 3 times as often
in the lowest income category as in the highest income cate-
gory, whereas depressive disorders occur only about 1.5
times as often in the lowestincomecategory as in the highest
income category (Kessler & Zhao, 1999; Monroe et al., 2009).
social - maladaptive peer relationships
bullying
sources of popularity vs rejection
In summary, children who fail to establish satisfactory
relationships with peers during the developmental years
are deprived of a crucial set of background experiences
and are at higher-than-average risk for a variety of nega-
tive outcomes in adolescence and adulthood including
depression, school dropout, suicidal ideation, and delin-
quency (Heilbron & Prinstein, 2010). However, one should
also remember that peer social problems may also be early
markers of disorders that have a heritable component but
do not become full blown until later in adolescence or
adulthood.
social - prejudice, discrimination in race, gender and ethnicity
Experimental laboratory studies have tested how prej-
udice and discrimination may “get under the skin” to
increase the likelihood of negative health outcomes. Such
studies have shown that the experience or perception of
racial discrimination leads to increases in anger and car-
diovascular reactivity (Mendes et al., 2008). In addition,
discrimination increases risk-taking behavior, an effect that
is partially mediated (or explained) by increased cardio-
vascular reactivity (Jamieson et al., 2013). Perceived dis-
crimination also predicts lower levels of well-being for
women (Ryff et al., 2003).
cultural perspective
The cultural perspective is concerned with the impact
of culture on the definition and manifestation of mental
disorders.
Research supports the view that many psychological
disturbances—in both adults and children—are universal,
appearing in most cultures studied (Butcher, 2005; Kessler
& Ustun, 2008).
Although some universal symptoms and patterns of
symptoms appear, sociocultural factors often influence
which disorders develop, the forms they take, how preva-
lent they are, and their courses.
Beyond differences in how symptoms are expressed or
reported by the individual, cultural differences in psycho-
pathology may also result from differences in what cul-
tures consider to bethe ideal kinds of behavior by members
of that society.
eating disorder
According to the DSM-5 (APA, 2013), eating disorders
are characterized by a persistent disturbance in eating
behavior.
clinical aspects of eating disorders - anorexia nervosa
An important change from DSM-IV
to DSM-5 is that in DSM-5 amenorrhea (cessation of men-
struation) is no longer required for a person to be given the
diagnosis. Studies have suggested thatwomen whocontinue
to menstruate but meet all the other diagnostic criteria for
anorexia nervosa are very similar psychologically to women
who have amenorrhea and have ceased menstruating (Attia
& Roberto, 2009). Amenorrhea is also not a cri-
terion that can be used for males, nor can it be
assessed in prepubescent girls or in women
who use hormonal contraceptives.
dsm 5 criteria
A. Restriction ofenergy intake relative to requirements, leading
to a significantly low body weight in the context of age, sex,
developmental trajectory, and physical health. Significantly
low weight is defined as a weight that is less than minimally
normal or, for children and adolescents, less than that min-
imally expected.
B. Intense fear of gaining weight or of becoming fat, or persis-
tent behavior that interferes with weight gain, even though
at a significantly low weight.
C. Disturbancein the wayin which one’s body weight or shape
is experienced, undue influence of body weight or shape on
self-evaluation, or persistent lack of recognition of the seri-
ousness of the current low body weight.
There are two types of anorexia nervosa: the restricting
type and the binge-eating/purging type. The central differ-
ence between these two subtypes concerns the way in
which patients maintain their very low weight. In the
restricting type, every effort is made to limit the quantity of
food consumed. Patients with the
binge-eating/purging type of anorexia nervosa differ
from patients with restricting anorexia nervosa because in
addition to restrictive eating, they also either binge eat,
purge, or binge eat and purge.
bulimia nervosa
Bulimia nervosa is characterized by uncontrollable binge
eating and efforts to prevent resulting weight gain by using
inappropriate behaviors such as self-induced vomiting and
excessive exercise. Bulimia nervosa was recognized as a
psychiatric syndrome relatively recently. The British psy-
chiatrist G. F. M. Russell (1997) proposed the term in 1979,
and it was adopted into the DSM in 1987. The word bulimia
comes from the Greek bous (which means “ox”), and limos
(“hunger”). It is meant to denote a hunger of such propor-
tions that the person “could eat an ox.”
The DSM-5 criteria
A. Recurrent episodes of binge eating. An episode of binge eat-
ing is characterized by both of the following:
1. Eating, in adiscrete period of time (e.g., within any 2-hour
period), an amount of food that is definitely larger than
what most individuals would eat in a similar period of
time under similar circumstances.
2. 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).
B. Recurrent inappropriate compensatory behaviors in order to
prevent weight gain, such as self-induced vomiting; misuse of
laxatives, diuretics, or other medications; fasting; or excessive
exercise.
C. The binge eating and inappropriate compensatory behaviors
both occur, on average, at least once a week for 3 months.
D. Self-evaluation is unduly influenced by body shape and
weight.
E. The disturbance does not occur exclusively during episodes of
anorexia nervosa.
People with anorexia nervosa and bulimia nervosa
share a common preoccupation with their shape and
their weight. However, unlike patients with anorexia
nervosa, those with bulimia nervosa are typically of nor-
mal weight or sometimes even slightly overweight.
binge-eating disorder
A new addition to DSM-5 is the diagnosis of binge-eating
disorder (BED). BED has some clinical features in com-
mon with bulimia nervosa (see the DSM-5 criteria box).
However, there is an important difference. After a binge,
the person with BED does not engage in any form of inap-
propriate “compensatory” behavior such as purging,
using laxatives, or even exercising to limit weight gain.
(Table 9.2 summarizes the similarities and differences
between different types of eating disorders.)
There is also much less dietary restraint in BED than is
typical of either bulimia nervosa or anorexia nervosa
(Wilfley et al., 2000). A typical binge averages around 1,900
calories (Bartholme et al., 2006). Not surprisingly, binge
eating disorder is associated with being overweight or
even obese (Hudson et al., 2007; Pike et al., 2001), although,
as with bulimia nervosa, weight is not a factor involved in
making the diagnosis.
DSM-5 Criteria for. . .
Binge-Eating Disorder
A. Recurrent episodes of binge eating. An episode of binge
eating is characterized by both of the following:
1. Eating, in a discrete period of time (e.g., within any
2-hour period), an amount of food that is definitely
larger than what most people would eat in a similar
period of time under similar circumstances.
2. A sense of lack of control over eating during the epi-
sode (e.g., a feeling that one cannot stop eating or
control what or how much one is eating).
B. The binge-eating episodes are associated with three (or
more) of the following:
1. Eating much more rapidly than normal.
2. Eating until feeling uncomfortably full.
3. Eating large amounts of food when not feeling physi-
cally hungry.
4. Eating alone because of feeling embarrassed by how
much one is eating.
5. Feeling disgusted with oneself, depressed, or very
guilty afterward.
C. Marked distress regarding binge eating is present.
D. The binge eating occurs, on average, at least once a week
for 3 months.
E. The binge eating is not associated with the recurrent use of
inappropriate compensatory behavior as in bulimia nervosa
and does not occur exclusively during the course of bulimia
nervosa or anorexia nervosa.
eating disorders - age of onset and gender differences
anorexia most likely in ages 16 - 20
bulimia women 21 - 24
binge eating 30 - 50
3 females for every male with an eating disorder
men are often under diagnosed
risk factor for men is homosexuality as value attractiveness more
prevalence of eating disorders
most common is binge eating - 3.5 % in women and 2 in men
bulimia - worldwide 1%
anorexia - in its severe form is as common as schizophrenia
medical complications of eating disorders
3% with anorexia die
- malnutrition
- thin and brittle hair
- dry skin
- yellowish skin
- difficulty in low temps
- low blood pressure so tired, weak dizzy and faint
- vitamin B1 deficiency
- irregular heartbeat
- dehydration
- kidney disease
- low potassium
- anemia
- loss of period
diagnostic crossover
One way in which eating disorders differ from other types
of disorders is that there is a lot of diagnostic crossover.
What this means is that it is quite common for someone
who is diagnosed with one form of eating disorder to be
later diagnosed with another eating disorder. This may
reflect the fact that current diagnostic systems are not
doing a good job categorizing these disorders and that
dimensionally based approaches might be more appropri-
ate.
association of eating disorders with other forms of psychopathy
Eating disorder diagnoses are commonly associated with
other diagnosable psychiatric conditions. In fact, comorbid-
ity is the rule rather than the exception (Hudson et al., 2007).
For instance, approximately 68 percent of patients with
anorexia nervosa, 63 percent of patients with bulimia ner-
vosa, and almost 50 percent of people with binge-eating dis-
order are also diagnosed with depression (Brewerton et al.,
1995; Halmi, et al., 1991; Hudson et al., 2007; O’Brian & Vin-
cent, 2003). Obsessive-compulsive disorder is often found in
patients with anorexia nervosa and bulimia nervosa (Kaye
et al., 2004; Milos et al., 2002; O’Brian & Vincent, 2003).
also substance abuse in binge eating, bulimia and anorexia
also personality disorders
eating disorders across cultures
Although the majority of research on eating disorders is
conducted in the United States and Europe, eating disor-
ders are not confined to these areas. Widespread eating
disorder difficulties have been reported among both Cau-casian and black South African college students (le Grange
et al., 1998).Anorexia nervosa and bulimia nervosa are also
clinical problems in Japan, Hong Kong, Taiwan, Singapore,
and Korea (Lee & Katzman, 2002).
Additionally, cases of eating disorders have been docu-
mented in India and Africa. The prevalence of eating disor-
ders in Iran is comparable to that in the United States
(Nobakht & Dezhkam, 2000). And a few years ago, the first
published report of five men in centralChina who were diag-
nosed with eating disorders appeared (Tong et al., 2005). Far
from being confined to industrialized Western countries, eat-
ing disorders are becoming a problem worldwide.
Being Caucasian, however, does appear to be associ-
ated with subclinical problems that may place individuals
at higher risk for developing eating disorders. Examples of
such problems include body dissatisfaction, dietary
restraint, and a drive for thinness. A meta-analysis involv-
ing a total of 17,781 participants has shown that such atti-
tudes and behaviors are significantly more prevalent in
whites than in nonwhites (Wildes et al., 2001).
Although Asian women exhibit levels of pathological
eating similar to those of white women (Wildes et al.,2001),
it has long been held that African Americans are less sus-
ceptible to subclinical types of eating problems and body
image concerns than Caucasians are.
risk and causal factors In eating disorders
biological, sociocultural, family and individual variables all play a part.
biological
- genetics - no evidence for link of candidate genes , the risk id higher if runs in family
- Brain abnormalities - hypothalamus as plays and important role in eating eg tumours in hypothalamus associated with increase or loss of appetite
- set point - There is a well-established tendency for our
bodies to resist marked variation from some sort of biolog-
ically determined set point or weight that our individual
bodies try to “defend” - serotonin - it modulates appetite and feeding behaviour , many patients reposed well to treatment with antidepressants
- reward sensitivity - A new direction in eating disor-
ders research centers onthe brain pathways and neurotrans-
mitters (such as dopamine) that are involved in reward
processing. This makes a lot of sense because individuals
who binge eat tend to consume high-fat and high-sugar
foods that most of us tend to think of as rewarding. In con-
trast, being less sensitive to food reward may make it easier
for some people to restrict their food intake, thereby increas-
ing risk for the development of anorexia nervosa (Stice &
Shaw, 2017).
sociocultural
- thinness being deeply rooted as a cultural ideal
- media creating pressure s to be thin
eg after TV went to Fiji women more concerned about their weight
family
- family dysfunction is a risk factor
- high parental expectations
- other family members dieting
- degree of critical comments from
other family members about shape, weight, or eating.
individual risk factors
gender - more frequent in women
internalising the thin ideal - extent to which people do this is associated with a body dissatisfaction, dieting and negative affect.
perfectionism - think thin body is the ideal ‘perfect body’
negative body image - consequence of sociocultural pressures
dieting - a risk factor of development or worsening of eating disorders
negative emotionality - negative affect as when we feel bad we become self-critical, it also predicts dietary restraint
treatment of anorexia
medications eg antidepressants, antipsychotic - olonzapine
family therapy - good for adolescents - better if il for under 3 years
CBT - for 1 to 2 years - modify distorted beliefs about weight and food
treatment of bulimia
medications - antidepressants
CBT - focuses on normalising eating patterns with meal plans, nutritional education and ending binging and purging cycles by teaching person to eat small amounts regulary
treatment for binge eating
antidepressants, appetite supplements and anticonvulsant medications
interpersonal therapy or CBT
obesity
defined based on the statistic of the body mass index.
obesity medical issues and prevalence
high cholesterol, hypertension, heart disease, arthritis, diabetes and cancer
prevalence has doubled since 1980 - 600m adults are obese
weight stigma
people who are obese are often judged harshly by others. in the media are presented more negatively and are less likely to be shown having romantic relationships.
obesity and DSM
not included in DSM 5 and not an eating disorder from a diagnostic perspective
risk and causal factors obesity - genes
In all probability our genetic makeup plays
an important role in determining how predisposed we are
to becomingobese in the modern environment of increased
food availability. Some of the genes that may, in our ances-
tral past, have been advantageous and helped us survive
in times of famine may predispose those who carry them
to readily gain weight when food is plentiful. Interestingly,
population groups that were most susceptible to starva-
tion throughout history (e.g., Pima Indians, Pacific Island-
ers) are those that are most inclined to become obese when
they have a sedentary lifestyle and a Western diet (see
Friedman, 2003).
evidence suggests BMI is polygenic and is influenced by a large number of common genes
hormones involved in appetite and weight regulation
leptin - Leptin (the name comesfrom the Greek
word leptos, meaning “thin”) is produced by fat cells. It
provides a key metabolic signal that informs the central
nervous system about the state of the body’s fat reserves.
When body fat levels decrease, leptin production decreases
and food intake is stimulated (Ravussin et al., 2014). Rare
genetic mutations that result in an inability to produce
leptin cause people to have an insatiable appetite and
result in morbid obesity. but has little effect as a treatment
gherlin - Ghrelin (the name comes
from a Hindu word meaning “growth”) is a hormone that
is produced by the stomach. It is a powerful appetite stimulator. Under normal circumstances, ghrelin levels rise
before a meal and fall after we have eaten. When ghrelin is
injected into human volunteers, it makes them very hun-
gry. This suggests that ghrelin is a key contributor to the
appetite control system.
People with a rare condition called Prader–Willi syn-
drome have chromosomal abnormalities that create many
problems, one of which is very high levels of ghrelin. Suf-
ferers are extremely obese and often die before age 30 from
obesity-related causes.
sociocultural influences
living in a culture that provides
ready access to high-fat, high-sugar (junk) foods, encour-
ages overconsumption, and makes it easy to avoid exercise.
Consider also the issue of accessibility. Foods with
low nutritional value (high fat, high sugar) are less expen-
sive and also much easier to find than foods with high
nutritional value.
Continued exposure to a culture that provides easy
access to highly palatable foods, offers large portions, and
bombards people with endless food advertisements may
explain why rates of obesity increase in immigrants after
they have lived in the United States for a while.
family influences
Family behavior patterns may also play a role in the devel-
opment of excessive eating and obesity. In some families, a
high-fat, high-calorie diet (or an overemphasis on food)
may lead to obesity in many or all family members,
including the family pet. In other families, eating (or over-
eating) becomes a habitual means of alleviating emotional
distress or showing love (Musante et al., 1998).
Family attitudes toward food are important because
their consequences are likely to remain with us for a long
time.
stress and comfort food
Foods that are high in fat
or carbohydrates are the foods that console most of us
when we are feeling troubled (Canetti et al., 2002). Workers
who say that they are under a lot of stress report that they
eat less healthy foods, and foods that are higher in fat, rela-
tive to their less stressed counterparts (Ng & Jeffery, 2003).
Might overeating function as a means of reducing feel-
ings of distress or depression? Certainly many people with
obesity experience psychological problems such as depres-
sion.
pathways to obesity
Understanding the causes of obesity is complex because it
results from a combination of genetic, environmental, and
sociocultural influences. An important step along the path-
way to obesity, however, may be binge eating. In a pro-
spective study of 231 adolescent girls, Stice and colleagues
(2002) established that binge eating is a predictor of later
obesity. This suggests that we should pay close attention to
the causes of binge eating.
Relevant here is research suggesting that one pathway
to binge eating may be through social pressure to conform
to the thin ideal, as ironic as this may seem (Stice et al.,
2002). Being heavy often leads to dieting, which may lead
to binge eating when willpower wanes. Another pathway
to binge eating may operate through depression and low
self-esteem.
importance of prevention
Reducing the prevalence of obesity is now a top priority.
But if obesity is to be prevented, it must first be recognized.
Astonishingly, in a recent study conducted in Finland,
57 percent of parents who had a 7-year-old child who was
overweight or obese failed to recognize that their child was
overweight (Vanhala et al., 2009). In this Finnish study,
childhood obesity was predicted by having a parent with
obesity, skipping breakfast, habitual overeating, and not
being physically active. Because we know that childhood
obesity predicts adult obesity, parental education is clearly
very important.
treatments of obesity
- lifestyle modifications - low calorie diet, exercise and some form of behavioural intervention
-medications - orlistat works by reducing the amount of fat in the diet that can be
absorbed onceit enters the gut. Other drugs such as lorcase-
rin (Belviq) work in different ways and target serotonin or
other neurotransmitters. The newest medication to receive
FDA approval is Contrave. This is a combination of naltrex-
one (used to treat drug and alcohol addiction) and bupro-
pion (used to treat depression and to help smokers quit). - bariatric surgery or gastric bypass surgery - most effective long term treatment - reduce storage and capacity of stomach and sometimes shorten length of intensitine so less food can be absorbed
