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Wednesday, February 2, 2011


With a basis for understanding how to define abnormal behaviour, we can focus on its causes. Abnormal behaviour isconstrued from a number of different perspectives. Each of the following models tells us something about different aspects of a multi-faceted group of mental disorders.Comorbidity is the occurrence of two or more disorders atthe same time.
Biological and genetic models assert that mental disorders are diseases, and symptoms of mental disorders are caused by factors such as brain defects (abnormalities in the structures of the brain), biochemical imbalances (complex dysregulation processes involving various neurotransmitters) and genetic predispositions (risk for psychopathology carried via our genetic material). By and large, the evidence for brain defects and biochemical imbalances as causes of mental disorders is correlational, which means that, although we know that such biological problems occur among people with mental disorders, we don’t know whether they actually cause the disorder. Because the brain is a fairly malleable organ, our behaviour and experiences can also affect our brain functioning, suggesting that the association between biology and abnormal behaviour may be reciprocal rather than unidirectional. Genetic models of mental disorder suggest that psychopathology is inherited from parents, and there is certainly evidence for the familial transmission of many disorders. For example, monozygotic (identical) twins
should be more likely than dizygotic (fraternal) twins to have the same disorder because they share 100 per cent of their genetic material, whereas dizygotic twins share only 50 per cent. For many disorders, this is exactly what research shows. But given that monozygotic twins share 100 per cent of their genetic material, you might expect them to have the same disorders 100 per cent of the time. But in fact they have the same disorders only about 50 per cent of the time. These findings have led researchers to conclude that, rather than being deterministic,genetics contributes about 50 per cent of the risk for mental illness. Such findings show that it doesn’t make sense to question whether mental illness is a function of nature or nurture. Instead we need to focus on how the two interact.

Freud emphasized the role of the early parent–child relationship in the development of mental illness. According to Freud, to the extent that the child did not successfully negotiate the psychosexual stages (see chapter 14), mental illness would develop. But Freud didn’t focus on what actually occurred in the parent– child relationship (e.g. whether parents were actually poor caretakers). Instead, his focus was on the unconscious internal desires and motivations of the child (e.g. sexual and aggressive impulses) and how the child negotiated them as s/he progressed through the early relationship with the child’s parents. For example, if an adult male found himself unable to deal with authority figures, this might be interpreted as unresolved aggressive impulses towards his father. Whether his father behaved as a harsh authority figure or not would be considered less relevant. So, according to Freud, mental illness is due to intrapsychic (i.e. within the mind) conflict. This means a person may have very little insight into the ‘true’ causes of their symptoms, as these are thought to be occurring at an unconscious level of processing. Many of Freud’s ideas have gone unsupported by research, but a number of them have proven to be fairly accurate. For example, there is ample evidence that people experience and process things at a non-conscious level (see Westen, 1998; also chapter 14) and that early interpersonal experiences affect later outcomes. In fact, this latter hypothesis became central to contemporary psychodynamic models of abnormal behaviour. Contemporary psychodynamic models (e.g., Kohut, 1977; Kernberg, 1976; Mitchell, 1988) also suggest that the early parent–child relationship is the original source of mental illness, and that what goes on in the mind of the child (and the adult) is important. But these models differ from Freud’s in that they focus more on interpersonal relationships than on intrapsychic conflict. These later models suggest that the early relationship between the child and the primary caregiver is crucial to the development of the self-concept, concepts of others, and the quality of relationships throughout life. The idea is that this early caregiver– child relationship is internalized by children, so that they learn about themselves and others from the manner in which the caregiver treats them. According to this framework, the nature of this internalized relationship and its resulting impact on the sense of self and the sense of others is what can create vulnerability to psychological problems.

The attachment model of psychopathology, developed by Bowlby (1969; 1973; 1980; see also chapter 9) resembles the contemporary psychodynamic models in that it also emphasizes the early parent–child relationship and how the resulting models of self and others guide development. But rather than being interested in people’s perceptions of their early experience, Bowlby was interested in the actual characteristics of the relationship. He relied on observational studies of parents and children to build his theory, rather than on retrospective reports of adults. The theory therefore has a strong empirical foundation.
Attachment theory suggests that when parental behaviour fails to make children feel safe, secure, and able to turn to and trust the parent in times of need, then children will be unable to regulate their emotions and needs adaptively and will develop negative, ‘insecure’ views of themselves and others. This would put children at risk for developing psychological disorders.
Research supports this hypothesis, as ‘insecure’ children and adults show more psychopathology than ‘secure’ children and adults (see Dozier,Stovall & Albus, 1999; Greenberg, 1999).biochemical imbalance complex neurotransmitterdysregulation process involving the various neurotransmitters in the braingenetic predisposition likelihood of showing condition or characteristic carried by genetic material familial transmission genetic transmission of disorders.

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