lecture 4 - mental health disorders 2 Flashcards
(67 cards)
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.