Approaches to trait anxiety(Cognitive)
The individual differences in the personality dimension of trait anxiety can be understood in part within a cognitive framework. The individuals high in trait anxiety possess various cognitive biases (e.g. attentional bias; interpretive bias) which lead them to exaggerate the threateningness of external and internal stimuli. These cognitive biases have recently been shown to have causal effects on individuals’ level of experienced anxiety. The original cognitive approach to trait anxiety was limited, because no distinction was drawn between two types of individuals scoring low on trait anxiety: (a) the truly low-anxious, who are non-defensive; (b) repressers, who are defensive. There is accumulating evidence that repressors possess opposite attentional and interpretive biases leading them to minimize the threateningness of external and internal stimuli. In contrast, the truly low-anxious do not possess cognitive biases or opposite cognitive biases. The represser group is of particular theoretical significance, because repressers show large discrepancies across the three major domains in which anxiety is assessed: self-report; behavioural; and physiological. These discrepancies depend on repressers’ opposite cognitive biases. It will be important in future research to integrate the cognitive approach to trait anxiety with a biological approach emphasizing the role of genetic factors in producing individual differences in trait anxiety.
There are five main personality factors, often referred to as the ‘Big Five’. The research of Goldberg was influential in establishing five major factors, but the most influential theorists to emphasize the Big Five have probably been. According to their approach, the five factors are neuroticism, extraversion, agreeableness, conscientiousness and openness to experience. Five personality factors, which has been variously described as neuroticism or trait anxiety. Neuroticism and trait anxiety overlap substantially with each other, as a result of which measures of the two dimensions typically correlate about +0.7 with each other .The key difference between them is that trait anxiety correlates negatively with extraversion, whereas neuroticism typically does not.. More generally,there is convincing evidence that most measures of trait anxiety and neuroticism (as well as measures of depression) correlate highly with a personality dimension sometimes labelled negative affectivity (Watson and Clark, 1984).
The approach adopted by most advocates of the Big Five factor approach to personality has focused on description rather than explanation. In general, there has been more progress in terms of identifying the structure of human personality than there has in terms of understanding the underlying mechanisms associated with individual differences along each of the dimensions identified.
The biological approach adopted by H.J.Eysenck and by Gray has received inconsistent support from psychological research. So far as the hypothesis that two-thirds of individual differences in neuroticism or trait anxiety are attributable to heredity is concerned, one of the most thorough studies (with many twins brought up apart) was the one reported by Pedersen et al. (1988). They assessed neuroticism in 95 monozygotic twin pairs brought up apart, 150 monozygotic twin pairs brought up together, 220 pairs of dizygotic twins brought up apart, and 204 pairs of dizygotic twins brought up together. They found that monozyotic twins brought up together had a correlation of +0.41, against +0.24 for dizygotic twins brought up together. For twins brought up apart, the correlations were +0.25 for monozygotic twins and +0.28 for dizygotic twins. These figures suggest that about 31 per cent of individual differences in neuroticism depend on genetic influences. However, the mean age of Pedersen et al’s sample (58.6 years) was higher than in most other studies, and a recent review has suggested that about 40 to 50 per cent of individual differences in neuroticism depend on genetic influences (Bouchard and Loehlin, 2001). The findings from twin studies indicate that genetic influences account for half (or a little less than half) of individual differences in neuroticism or trait anxiety. Thus, it is clearly important to consider environmental factors in order to achieve a good understanding of neuroticism or trait anxiety. a review of all of the available evidence, and came to the following pessimistic conclusion: ‘Over many decades research has failed to substantiate the physiological correlates that are assumed for emotionality and trait anxiety. There is virtually no distinct finding that has been reliably replicated across studies and laboratories.’ The evidence from empirical research demonstrating the limitations of the biological approach produced a situation in which there was no overall theory of trait anxiety and neuroticism which appeared adequate. However, the situation has changed to some extent in recent years. One of the main themes of this chapter is to argue that many of the limitations of the biological approach stem from its failure to consider seriously the role played by the cognitive system. It is increasingly recognized by personality researchers that an understanding of cognitive processes and structures can serve to enrich theories of personality (McCann and Endler, 2000). As will be seen, there is compelling evidence that there are systematic differences in cognitive functioning between individuals high and low in trait anxiety. More speculatively, these individual differences in cognitive functioning can be regarded as providing a partial explanation for the limitations of the biological approach. The remainder of this chapter is devoted to a consideration of cognitive approaches to trait anxiety, with the ultimate goal being to combine such approaches with the earlier biological approach.
The individual differences in the personality dimension of trait anxiety can be understood in part within a cognitive framework. The individuals high in trait anxiety possess various cognitive biases (e.g. attentional bias; interpretive bias) which lead them to exaggerate the threateningness of external and internal stimuli. These cognitive biases have recently been shown to have causal effects on individuals’ level of experienced anxiety. The original cognitive approach to trait anxiety was limited, because no distinction was drawn between two types of individuals scoring low on trait anxiety: (a) the truly low-anxious, who are non-defensive; (b) repressers, who are defensive. There is accumulating evidence that repressors possess opposite attentional and interpretive biases leading them to minimize the threateningness of external and internal stimuli. In contrast, the truly low-anxious do not possess cognitive biases or opposite cognitive biases. The represser group is of particular theoretical significance, because repressers show large discrepancies across the three major domains in which anxiety is assessed: self-report; behavioural; and physiological. These discrepancies depend on repressers’ opposite cognitive biases. It will be important in future research to integrate the cognitive approach to trait anxiety with a biological approach emphasizing the role of genetic factors in producing individual differences in trait anxiety.
There are five main personality factors, often referred to as the ‘Big Five’. The research of Goldberg was influential in establishing five major factors, but the most influential theorists to emphasize the Big Five have probably been. According to their approach, the five factors are neuroticism, extraversion, agreeableness, conscientiousness and openness to experience. Five personality factors, which has been variously described as neuroticism or trait anxiety. Neuroticism and trait anxiety overlap substantially with each other, as a result of which measures of the two dimensions typically correlate about +0.7 with each other .The key difference between them is that trait anxiety correlates negatively with extraversion, whereas neuroticism typically does not.. More generally,there is convincing evidence that most measures of trait anxiety and neuroticism (as well as measures of depression) correlate highly with a personality dimension sometimes labelled negative affectivity (Watson and Clark, 1984).
The approach adopted by most advocates of the Big Five factor approach to personality has focused on description rather than explanation. In general, there has been more progress in terms of identifying the structure of human personality than there has in terms of understanding the underlying mechanisms associated with individual differences along each of the dimensions identified.
The biological approach adopted by H.J.Eysenck and by Gray has received inconsistent support from psychological research. So far as the hypothesis that two-thirds of individual differences in neuroticism or trait anxiety are attributable to heredity is concerned, one of the most thorough studies (with many twins brought up apart) was the one reported by Pedersen et al. (1988). They assessed neuroticism in 95 monozygotic twin pairs brought up apart, 150 monozygotic twin pairs brought up together, 220 pairs of dizygotic twins brought up apart, and 204 pairs of dizygotic twins brought up together. They found that monozyotic twins brought up together had a correlation of +0.41, against +0.24 for dizygotic twins brought up together. For twins brought up apart, the correlations were +0.25 for monozygotic twins and +0.28 for dizygotic twins. These figures suggest that about 31 per cent of individual differences in neuroticism depend on genetic influences. However, the mean age of Pedersen et al’s sample (58.6 years) was higher than in most other studies, and a recent review has suggested that about 40 to 50 per cent of individual differences in neuroticism depend on genetic influences (Bouchard and Loehlin, 2001). The findings from twin studies indicate that genetic influences account for half (or a little less than half) of individual differences in neuroticism or trait anxiety. Thus, it is clearly important to consider environmental factors in order to achieve a good understanding of neuroticism or trait anxiety. a review of all of the available evidence, and came to the following pessimistic conclusion: ‘Over many decades research has failed to substantiate the physiological correlates that are assumed for emotionality and trait anxiety. There is virtually no distinct finding that has been reliably replicated across studies and laboratories.’ The evidence from empirical research demonstrating the limitations of the biological approach produced a situation in which there was no overall theory of trait anxiety and neuroticism which appeared adequate. However, the situation has changed to some extent in recent years. One of the main themes of this chapter is to argue that many of the limitations of the biological approach stem from its failure to consider seriously the role played by the cognitive system. It is increasingly recognized by personality researchers that an understanding of cognitive processes and structures can serve to enrich theories of personality (McCann and Endler, 2000). As will be seen, there is compelling evidence that there are systematic differences in cognitive functioning between individuals high and low in trait anxiety. More speculatively, these individual differences in cognitive functioning can be regarded as providing a partial explanation for the limitations of the biological approach. The remainder of this chapter is devoted to a consideration of cognitive approaches to trait anxiety, with the ultimate goal being to combine such approaches with the earlier biological approach.
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