Unit 2 B
Viewpoints for Understanding
the Causes of Abnormal
Behaviour; Biological
Viewpoint
The more complex the phenomenon being investigated, the greater the number of viewpoints that
develop in an attempt to explain it, although inevitably they are not all equally valid.
A particular viewpoint helps researchers and theoreticians to organize the observations they have made,
provides a system of thought in which to place the observed data, and suggests areas of focus for
research and treatment.
Fundamentally, viewpoints also help determine the kinds of potential causes that are even examined in
the first place.
However, that each of these viewpoints is a theoretical construction devised to orient psychologists in
the study of abnormal (and normal) behavior.
One potential problem is that when adherents of a particular viewpoint are overly confident about the
validity of that viewpoint, they may become blind to alternative interpretations.
Sigmund Freud helped shift the focus of abnormal psychology from biological illness or moral infirmity to
unconscious mental processes within the person.
In recent years, three other shifts in focus seem to have been occurring in parallel in the study of abnormal
behavior.
1. Biological viewpoint
2. Behavioral and cognitive-behavioral viewpoints
3. Sociocultural viewpoint
In the long run, however, we also know from biological, psychological, and sociocultural research that only
an integrated approach is likely to provide anything close to a full understanding of the origins of
various forms of psychopathology or the form that a long-lasting cure for many serious forms of
psychopathology might take. Thus, in recent years, many theorists have come to recognize the need for a
more integrative, biopsychosocial viewpoint that acknowledges that biological, psychological, and
sociocultural factors all interact and play a role in psychopathology and treatment.
BIOLOGICAL VIEWPOINT
Biological viewpoint is an approach to mental disorders emphasizing biological causation.
We will focus here on four categories of biological factors that seem particularly relevant to the
development of maladaptive behavior:
1. Neurotransmitter and hormonal abnormalities in the brain or other parts of the central nervous
system,
2. Genetic vulnerabilities,
3. Temperament,
4. Brain dysfunction and neural plasticity.
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.
Imbalances of Neurotransmitters
and Hormones
In order for the brain to function adequately, neurons, or nerve cells, need to be able to communicate effectively with one
another.
Nerves are bundles of axons coated in myelin that travel together through the body.
Nervous system is an extensive network of specialized cells that carries information to and from all parts of the body.
Neuron is the basic cell that makes up the nervous system and that receives and sends messages within that system. It
is a specialized cell for neural communication.
Dendrites: branchlike structures of a neuron that receive messages from other neurons.
Soma: the cell body of the neuron responsible for maintaining the life of the cell.
Axon: tube-like structure of neuron that carries the neural message from the cell body to the axon terminals, for
communication with other cells.
Axon Terminals: enlarged ends of axonal branches of the neuron, specialized for communication between cells.
Synapse (synaptic gap): microscopic fluid-filled space between the axon terminal of one cell and the dendrites or
surface of the next cell.
Synaptic vesicles saclike structures found inside the synaptic knob containing chemicals.
Receptor sites: three-dimensional proteins on the surface of the dendrites or certain cells of the muscles and glands,
which are shaped to fit only certain neurotransmitters.
Neurotransmitter: A chemical found in the synaptic vesicles that, when released, has an effect on the next cell.
The neurotransmitter substances released into the synapse then 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.
The neurotransmitters can stimulate that postsynaptic neuron to either initiate an impulse or inhibit impulse
transmission. Both kinds of messages are important.
Once the neurotransmitter substance is released into the synapse, it does not stay around indefinitely
(otherwise, the receiving neuron would continue firing in the absence of a real impulse).
Sometimes the neurotransmitters are quickly destroyed by an enzyme such as monoamine oxidase, and
sometimes they are returned to storage vesicles in the axon endings by a reuptake mechanism—a process
of reabsorption by which the neurotransmitters are reabsorbed or effectively sucked back up into the axon
ending.
The enzyme monoamine oxidase is also present in the presynaptic terminal and can destroy excess
neurotransmitter there too.
There are many different kinds of neurotransmitters; some increase the likelihood that the postsynaptic
neuron will “fire” (produce an impulse), and others inhibit the impulse.
Whether the neural message is successfully transmitted to the postsynaptic neuron depends, among other
things, on the concentration of certain neurotransmitters within the synapse.
Imbalances of Neurotransmitter Systems
The belief that imbalances in neurotransmitters in the brain can result in abnormal behavior is one of the basic
tenets of the biological perspective. Sometimes psychological stress can bring on neurotransmitter
imbalances. These imbalances can be created in a variety of ways:
There may be excessive production and release of the neurotransmitter substance into the synapses,
causing a functional excess in levels of that neurotransmitter.
There may be dysfunctions in the normal processes by which neurotransmitters, once released into the
synapse, are deactivated. Ordinarily this deactivation occurs either through a process of reuptake of the
released neurotransmitter from the synapse into the axon endings or through a process of degradation by
certain enzymes that may be present in the synapse and in the presynaptic axon endings.
Finally, there may be problems with the receptors in the postsynaptic neuron, which may be either
abnormally sensitive or abnormally insensitive.
Although over a hundred neurotransmitters have been discovered to date, five different kinds of
neurotransmitters have been most extensively studied in relationship to psychopathology: (1)
norepinephrine, (2) dopamine, (3) serotonin, (4) glutamate, and (5) gamma aminobutyric acid. The first
three belong to a class of neurotransmitters called monoamines because each is synthesized from a single
amino acid (monoamine means “one amine”).
Norepinephrine has been implicated as playing an important role in the emergency reactions our bodies
show when we are exposed to an acutely stressful or dangerous situation, as well as in attention,
orientation, and basic motives.
Some of the functions of dopamine include pleasure and cognitive processing, and it has been implicated
in schizophrenia as well as in addictive disorders.
Serotonin has been found to have important effects on the way we think and process information from
our environment as well as on behaviors and moods. Not surprisingly, then, it seems to play an important
role in emotional disorders such as anxiety and depression, as well as in suicide. The excitatory
neurotransmitter glutamate, which has been implicated in schizophrenia.
The neurotransmitter GABA, is strongly implicated in reducing anxiety as well as other emotional states
characterized by high levels of arousal.
Hormonal Imbalances
Some forms of psychopathology have also been linked to hormonal imbalances. Hormones are
chemical messengers secreted by a set of endocrine glands in our bodies.
Each of the endocrine glands produces and releases its own set of hormones directly into our
bloodstream.
The hormone then travel and directly affect target cells in various parts of our brain and body,
influencing diverse events such as fight-or-flight reactions, sexual responses, physical growth,
and many other physical expressions of mental states.
Our central nervous system is linked to the endocrine system (in what is known as the
neuroendocrine system) by the effects of the hypothalamus on the pituitary gland, which is the
master gland of the body, producing a variety of hormones that regulate or control the other
endocrine glands.
One particularly important set of interactions occurs in the hypothalamic-pituitary-adrenal axis (HPA
axis). Activation of this axis involves:
1. Messages in the form of corticotrophin-releasing hormone (CRH) travel from the hypothalamus
to the pituitary.
2. In response to CRH, the pituitary releases adrenocorticotrophic hormone (ACTH), which
stimulates the cortical part of the adrenal gland (located on top of the kidney) to produce
epinephrine (adrenaline) and the stress hormone cortisol, which are released into general
circulation. Cortisol mobilizes the body to deal with stress.
3. Cortisol in turn provides negative feedback to the hypothalamus and pituitary to decrease their
release of CRH and ACTH, which in turn reduces the release of adrenaline and cortisol. This
negative feedback system operates much as a thermostat does to regulate temperature.
Malfunctioning of this negative feedback system has been implicated in various forms of
psychopathology such as depression and posttraumatic stress disorder.
Genetic Vulnerabilities
The biochemical processes are themselves affected by genes, which consist of very long
molecules of DNA (deoxyribonucleic acid) and 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 genetic information that we inherit from our parents and other ancestors, and
each gene exists in two or more alternate forms called alleles.
Neither behavior nor mental disorders are ever determined exclusively by genes, there is
substantial evidence that most mental disorders show at least some genetic influence ranging
from small to large. Some of these genetic influences, such as broad temperamental features, are
first apparent in newborns and children. Example: Some children are just naturally more shy or
anxious, whereas others are more outgoing.
However, some genetic sources of vulnerability do not manifest themselves until adolescence or
adulthood, when most mental disorders appear for the first time.
Healthy human cells have 46 chromosomes containing genetic materials that encode the hereditary plan
for each individual, providing the potentialities for development and behavior of that individual throughout
a lifetime. The normal inheritance consists of 23 pairs of chromosomes, one of each pair 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, determine the individual’s sex. In a female, both of these sex
chromosomes—one from each parent—are designated as X chromosomes. In a male, the sex chromosome
from the mother is an X, but that from the father is a Y chromosome.
Abnormalities in the structure or number of the chromosomes can be associated with major defects or
disorders. Down syndrome is a type of intellectual disability (also associated with recognizable facial
features such as a flat face and slanted eyes) in which there is a trisomy (a set of three chromosomes
instead of two) in chromosome 21. Here the extra chromosome is the primary 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 a person to develop abnormal behavior.
Personality traits and mental disorders are not affected by chromosomal abnormalities per se.
Instead they are more often influenced either by abnormalities in some of the genes on the
chromosomes or by naturally occurring variations of genes known as polymorphisms.
Gene “expression” is normally not a simple outcome of the information encoded in DNA but 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
The Relationship of Genotypes to Phenotypes
A person’s total genetic endowment is referred to as her or his genotype and, except for identical twins, no
two humans ever begin life with the same endowment.
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.
In some cases, the genotypic vulnerability present at birth does not exert its effect on the phenotype until
much later in life. In many other cases, the genotype may shape the environmental experiences a child has,
thus affecting the phenotype in yet another very important way.
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 adolescence.
Methods for Studying Genetic Influences
Although advances are beginning to be made in identifying faulty genetic endowment, for the
most part we are not yet able to isolate, on the genes themselves, specific defects for mental
disorders.
Therefore, most of the information we have on the role of genetic factors in mental disorders is
based not on studies of genes but on studies of people who are related to each other.
Three primary methods have traditionally been used in behavior genetics, the field that focuses
on studying the heritability of mental disorders (as well as other aspects of psychological
functioning): (1) the family history (or pedigree) method, (2) the twin method, and (3) the
adoption method. More recently, two additional methods, linkage studies and association
studies, have also been developed.
Family history method. Behavior genetic research strategy that examines the incidence of disorder in relatives of
an index case to determine whether incidence increases in proportion to the degree of the hereditary relationship.
The main limitation of this method is that people who are more closely related genetically also tend to share more
similar environments, which makes it difficult to disentangle genetic and environmental effects.
Twin method. The use of identical and non-identical twins to study genetic influences on abnormal behavior. Thus
if a given disorder or trait were completely heritable, one would expect the concordance rate—the percentage of
twins sharing the disorder or trait—to be 100 percent. That is, if one identical twin had a particular disorder, the
other twin would as well.
There are relatively high concordance rates for identical twins in some more severe forms of psychopathology.
These concordance rates are particularly meaningful when they differ from those found for non-identical twins. For
most of the disorders, concordance rates are indeed much lower for non-identical twins than for identical twins.
Adoption method. Comparison of biological and adoptive relatives with and without a given disorder to assess
genetic versus environmental influences.
Linkage analysis. Genetic research strategy in which occurrence of a disorder in an extended family is compared
with that of a genetic marker for a physical characteristic or biological process that is known to be located on a
particular chromosome.
Association studies. Genetic research strategy comparing frequency of certain genetic markers known to be located
on particular chromosomes in people with and without a particular disorder.
Temperament
Temperament refers to pattern of emotional and arousal responses and characteristic ways of self-
regulation that are considered to be primarily hereditary or constitutional.
Our early temperament is thought to be the basis from which our personality develops.
Starting at about 2 to 3 months of age, approximately five dimensions of temperament can be identified:
fearfulness, irritability and frustration, positive affect, activity level, and attentional persistence and
effortful control. These seem to be related to the three important dimensions of adult personality: (1)
neuroticism or negative emotionality, (2) extraversion or positive emotionality, and (3) constraint
(conscientiousness and agreeableness).
The infant dimensions of fearfulness and irritability, which show few gender differences, correspond to
the adult dimension of neuroticism
The infant dimensions of positive affect and possibly activity level seem related to the adult dimension of
extraversion,
The infant dimension of attentional persistence and effortful control seem related to the adult dimension
of constraint or control.
The temperament of an infant or young child has profound effects on a variety of important
developmental processes.
Example: A child with a fearful temperament has many opportunities for the classical
conditioning of fear to situations in which fear is provoked; later the child may learn to avoid
entering those feared situations, and evidence suggests that he or she may be especially likely to
learn to fear social situations.
Children with high levels of positive affect and activity are more likely to show high levels of
mastery motivation, whereas 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. This seems to be true
especially in families with lower socioeconomic status, which are, on average, less supportive of
difficult children than families of mid to high socioeconomic status.
Temperament may also set the stage for the development of various forms of psychopathology
later in life.
Brain Dysfunction and Neural Plasticity
Specific brain lesions with observable defects in brain tissue 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 increased availability of sophisticated new neuroimaging
techniques to study the function and structure of the brain.
These and other kinds of techniques have shown that genetic programs for brain development are
not as rigid and deterministic as was once believed.
There is considerable neural plasticity—flexibility of the brain in making changes in organization
and function in response to pre- and postnatal experiences, stress, diet, disease, drugs, maturation,
and so forth. Existing neural circuits can be modified, or new neural circuits can be generated. The
effects can be either beneficial or detrimental to the individual, depending on the circumstances.
One example of the positive effects of prenatal experiences comes from an experiment in which pregnant rats housed
in complex, enriched environments had offspring that were less negatively affected by brain injury that occurred early
in development than those without the same positive prenatal experiences. One example of negative effects of prenatal
experiences comes from an experiment in which pregnant monkeys exposed to unpredictable loud sounds had infants
that were jittery and showed neurochemical abnormalities (specifically, elevated levels of circulating catecholamines).
Many postnatal environmental events also affect the brain development of the infant and child. The formation of new
neural connections (or synapses) after birth is dramatically affected by the experiences a young organism has. Rats
reared in enriched environments (as opposed to in isolation) show heavier and thicker cell development in certain
portions of the cortex (as well as more synapses per neuron). Similar but less extensive changes can occur in older
animals exposed to enriched environments; hence neural plasticity continues to some extent throughout the life span.
The early implications of this kind of work were taken to suggest that human infants should be exposed to highly
enriched environments. However, subsequent work has shown that normal rearing conditions with caring parents are
perfectly adequate. What later work really showed is that unstimulating, deprived environments can cause retarded
development.
This research on neural and behavioral plasticity, in combination with the work on genotype–environment correlations,
makes it clear why developmental psychopathologists have been devoting increasing attention to a developmental
systems approach. This approach acknowledges not only that genetic activity influences neural activity, which in turn
influences behavior, which in turn influences the environment, but also that these influences are bidirectional.
