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My thanks again go to my psychology and medical students and to my colleagues over the years for their comments and feedback 5mg clarinex. For this edition I am particularly grateful to Derek Johnston and Amanda Williams for pointing me in the right direction cheap 5 mg clarinex with visa, to David Armstrong for conversation and cooking, to Cecilia Clementi for help with all the new references and for Harry and Ellie for being wonderful and for going to bed on time. Take advantage of the study tools offered to reinforce the material you have read in the text, and to develop your knowledge of Health Psychology in a fun and effective way. Study Skills Open University Press publishes guides to study, research and exam skills, to help under- graduate and postgraduate students through their university studies. Get a £2 discount off these titles by entering the promotional code app when ordering online at www. The chapter highlights differences between health psychology and the biomedical model and examines the kinds of questions asked by health psychologists. Then the possible future of health psychology in terms of both clinical health psychology and becoming a professional health psychologist is discussed. Finally, this chapter outlines the aims of the textbook and describes how the book is structured. This chapter covers: ➧ The background to health psychology ➧ What is the biomedical model? Darwin’s thesis, The Origin of Species, was published in 1856 and described the theory of evolution. This revolutionary theory identified a place for Man within Nature and suggested that we were part of nature, that we developed from nature and that we were biological beings. This was in accord with the biomedical model of medicine, which studied Man in the same way that other members of the natural world had been studied in earlier years. This model described human beings as having a biological identity in common with all other biological beings. The biomedical model of medicine can be understood in terms of its answers to the following questions: s What causes illness? According to the biomedical model of medicine, diseases either come from outside the body, invade the body and cause physical changes within the body, or originate as internal involuntary physical changes. Such diseases may be caused by several factors such as chemical imbalances, bacteria, viruses and genetic predisposition. Because illness is seen as arising from biological changes beyond their control, individuals are not seen as responsible for their illness. The biomedical model regards treatment in terms of vaccination, surgery, chemotherapy and radiotherapy, all of which aim to change the physical state of the body. Within the biomedical model, health and illness are seen as qualitatively different – you are either healthy or ill, there is no continuum between the two. According to the biomedical model of medicine, the mind and body function independently of each other. From this perspective, the mind is incapable of influencing physical matter and the mind and body are defined as separate entities. The mind is seen as abstract and relating to feelings and thoughts, and the body is seen in terms of physical matter such as skin, muscles, bones, brain and organs. Changes in the physical matter are regarded as independent of changes in state of mind. Within traditional biomedicine, illness may have psychological consequences, but not psychological causes. These developments have included the emergence of psychosomatic medicine, behavioural health, behavioural medicine and, most recently, health psychology. These different areas of study illustrate an increasing role for psychology in health and a changing model of the relationship between the mind and body. Psychosomatic medicine The earliest challenge to the biomedical model was psychosomatic medicine. This was developed at the beginning of the twentieth century in response to Freud’s analysis of the relationship between the mind and physical illness. At the turn of the century, Freud described a condition called ‘hysterical paralysis’, whereby patients presented with paralysed limbs with no obvious physical cause and in a pattern that did not reflect the organization of nerves. Freud argued that this condition was an indication of the individual’s state of mind and that repressed experiences and feelings were expressed in terms of a physical problem. This explanation indicated an interaction between mind and body and suggested that psychological factors may not only be consequences of illness but may contribute to its cause. Behavioural health Behavioural health again challenged the biomedical assumptions of a separation of mind and body. Behavioural health was described as being concerned with the main- tenance of health and prevention of illness in currently healthy individuals through the use of educational inputs to change behaviour and lifestyle.

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She stated that smoking works to promote these women’s sense of well-being and to help them cope with caring cheap 5mg clarinex with amex. She reports that smoking can be seen as ‘the only activity they do buy cheap clarinex 5 mg, just for themselves’. Smoking is therefore a product not only of beliefs but also an individual’s social world. Alcohol initiation and maintenance Most people try alcohol at some time in their lives. The most common reasons for never drinking alcohol were religion and not liking it. Therefore, rather than examining predictors of drinking ‘ever’ or ‘occasionally’, this section examines what factors predict developing a problem with drinking. Psychological predictors of alcohol initiation and maintenance The tension-reduction hypothesis (Cappell and Greeley 1987) suggests that individuals may develop a drink problem because alcohol reduces tension and anxiety. However, it has been suggested that it is not the actual effects of alcohol use that promote drinking but the expected effects (George and Marlatt 1983). Therefore, because a small amount of alcohol may have positive effects people assume that these positive effects will continue with increased use. This perspective is in line with the social learning model of addictive behaviours and emphasizes the role of reinforcement and cognitions. Social predictors of alcohol initiation and maintenance Many of the social factors that relate to smoking behaviour are also predictive of alcohol consumption. According to a disease model of addictions it could be argued that this reflects the genetic predisposition to develop an addictive behaviour. However, parental drinking may be influential through ‘social hereditary factors’, with children being exposed to drinking behaviour and learning this behaviour from their parents (Orford and Velleman 1991). In addition, peer group alcohol use and abuse also predicts drinking behaviour as does being someone who is sensation seeking, with a tendency to be aggressive and having a history of getting into trouble with authority. Johnston and White (2003) used the theory of planned behaviour (see Chapter 2) to predict binge drinking in students. However, given the social nature of binge drinking they focused on the role of norms. Using a longitudinal design, 289 undergraduate students completed a questionnaire concerning their beliefs with follow-up collected about reported binge drinking. The results showed an important role for norms particularly if the norms were of a behaviourally relevant reference group that the student reported a strong identification with. Cessation of an addictive behaviour can be examined in terms of the processes involved in cessation and the interventions designed to motivate individuals to quit their behaviour. The process of cessation Traditionally, smoking cessation was viewed as a dichotomy: an individual either smoked or did not. This perspective was in line with a biomedical model of addictions and emphasized the ‘all or nothing nature’ of smoking behaviour. However, early attempts at promoting total abstinence were relatively unsuccessful and research now often emphasizes cessation as a process. In particular, Prochaska and DiClemente (1984; see Chapter 2) adapted their stages of change model to examine cessation of addictive behaviours. They argued that cessation involves a shift across five basic stages: 1 precontemplation: defined as not seriously considering quitting; 2 contemplation: having some thoughts about quitting; 3 preparation: seriously considering quitting; 4 action: initial behaviour change; 5 maintenance: maintaining behaviour change for a period of time. Prochaska and DiClemente maintain that individuals do not progress through these stages in a straightforward and linear fashion but may switch backwards and forwards (e. They call this ‘the revolving door’ schema and emphasize the dynamic nature of cessa- tion. This model of change has been tested to provide evidence for the different stages for smokers and outpatient alcoholics (DiClemente and Prochaska 1982; 1985; DiClemente and Hughes 1990), and for the relationship between stage of change for smoking cessa- tion and self-efficacy (DiClemente 1986). The authors categorized smokers into either precontemplators or contemplators and examined their smoking behaviour at follow-up. They further classified the contemplators into either contemplators (those who were smoking, seriously considering quitting within the next six months, but not within the next 30 days) or those in the preparation stage (those who were seriously considering quitting smoking within the next 30 days). The results showed that those in the prepara- tion stage of change were more likely to have made a quit attempt at both one and six months, that they had made more quit attempts, and were more likely to be not smoking at the follow-ups. Research has also used the health beliefs and structured models outlined in Chapter 2 to examine the predictors of both intentions to stop smoking and successful smoking cessation. For example, individual cognitions such as perceptions of susceptibility, past cessation attempts and perceived behavioural control have been shown to relate to reductions in smoking behaviour (Giannetti et al. The results showed that the best predictors of intentions to quit were perceived behavioural control (i.

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Evidence for these dimensions of illness cognitions The extent to which beliefs about illness are constituted by these different dimensions has been studied using two main methodologies – qualitative and quantitative research order clarinex 5 mg with mastercard. Qualitative research Leventhal and his colleagues carried out interviews with individuals who were chronically ill buy clarinex 5 mg online, had been recently diagnosed as having cancer, and with healthy adults. The resulting descriptions of illness suggest underlying beliefs that are made up of the above dimensions. Leventhal and his colleagues argued that interviews are the best way to access illness cognitions as this methodology avoids the possibility of priming the subjects. For example, asking a subject ‘to what extent do you think about your illness in terms of its possible consequences’ will obviously encourage them to regard con- sequences as an important dimension. However, according to Leventhal, interviews encourage subjects to express their own beliefs, not those expected by the interviewer. Quantitative research Other studies have used more artificial and controlled methodologies, and these too have provided support for the dimensions of illness cognitions. They asked 20 subjects to sort 65 statements into piles that ‘made sense to them’. They reported that the subjects’ piles of categories reflected the dimensions of identity (diagnosis/symptoms), consequences (the possible effects), time line (how long it will last), cause (what caused the illness) and cure/control (how and whether it can be treated). A series of experimental studies by Bishop and colleagues also provided support for these dimensions. For example, Bishop and Converse (1986) presented subjects with brief descriptions of patients who were experiencing six different symptoms. Subjects were randomly allocated to one of two sets of descriptions: high prototype in which all six symptoms had been previously rated as associated with the same disease, or low prototype in which only two of the six symptoms had been previously rated as associated with the same disease. The results showed that subjects in the high prototype condition labelled the disease more easily and accurately than subjects in the low prototype con- dition. The authors argued that this provides support for the role of the identity dimension (diagnosis and symptoms) of illness representations and also suggested that there is some consistency in people’s concept of the identity of illnesses. In addition, subjects were asked to describe in their own words ‘what else do you think may be associated with this person’s situation? They reported that 91 per cent of the given associations fell into the dimensions of illness representations as described by Leventhal and his colleagues. However, they also reported that the dimensions consequences (the possible effects) and time line (how long it will last) were the least frequently mentioned. There is also some evidence for a similar structure of illness representations in other cultures. Weller (1984) examined models of illness in English-speaking Americans and Spanish-speaking Guatemalans. The results indicated that illness was predominantly conceptualized in terms of contagion and severity. Hagger and Orbell (2003) carried out a meta analysis of 45 empirical studies which used Leventhal’s model of illness cognitions. They concluded from their analysis that there was consistent support for the different illness cognition dimensions and that the different cognitions showed a logical pattern across different illness types. Measuring illness cognitions Leventhal and colleagues originally used qualitative methods to assess people’s illness cognitions. These will be described in terms of questionnaires that have been developed and methodological issues surrounding measurement. This questionnaire asks subjects to rate a series of statements about their illness. This questionnaire has been used to examine beliefs about illnesses such as chronic fatigue syndrome, diabetes and arthritis and provides further support for the dimensions of illness cognitions (Weinman and Petrie 1997). However, people have beliefs not only about their illness but also about their treatment, whether it is medication, surgery or behaviour change. French and colleagues asked whether the form of method used to elicit beliefs about illness influ- enced the types of beliefs reported. Participants were asked either simply to rate a series of causes for heart attack (the questionnaire) or to read a vignette about a man and to estimate his chances of having a heart attack. The results showed that the two different methods resulted in different beliefs about the causes of heart attack and different importance placed upon these causes. Specifically, when using the questionnaire smoking and stress came out as more important causes than family history, whereas when using the vignette smoking and family history came out as more important causes than stress. The results showed stressors, fate or luck were more common beliefs about causes when using interval rating scales (i. These illness cognitions have been incorporated into a model of illness behaviour to examine the relationship between an individual’s cognitive repre- sentation of their illness and their subsequent coping behaviour. This model is based on approaches to problem solving and suggests that illness/symptoms are dealt with by individuals in the same way as other problems (see Chapter 4 for details of other models of problem solving). It is assumed that given a problem or a change in the status quo the individual will be motivated to solve the problem and re-establish their state of normality. Traditional models describe problem solving in three stages: (1) interpretation (making sense of the problem); (2) coping (dealing with the problem in order to regain a state of equilibrium); and (3) appraisal (assessing how successful the coping stage has been). According to models of problem solving these three stages will continue until the coping strategies are deemed to be successful and a state of equilibrium has been attained.

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Body dissatisfaction may well be an expression of this lack of control (Orbach 1978; Ogden 1999) buy 5mg clarinex amex. Herman and Mack 1975; Herman and Polivy 1984) was developed to evaluate the causes and consequences of dieting (referred to as restrained eating) and suggests that dieters show signs of both undereating and overeating purchase clarinex 5mg with mastercard. Dieting and undereating Restrained eating aims to reduce food intake and several studies have found that at times this aim is successful. This experimental method involves giving subjects either a high-calorie preload (e. After eating/drinking the preload, subjects are asked to take part in a taste test. The subjects are left alone for a set amount of time to rate the foods and then the amount they have eaten is weighed (the subjects do not know that this will happen). The aim of the preload/taste test method is to measure food intake in a controlled environment (the laboratory) and to examine the effect of preloading on their eating behaviour. Dieting and overeating In opposition to these findings, several studies have suggested that higher levels of restrained eating are related to increased food intake. For example, Ruderman and Wilson (1979) used a preload/taste test procedure and reported that restrained eaters consumed significantly more food than the unrestrained eaters, irrespective of pre- load size. In particular, restraint theory has identified the disinhibition of restraint as characteristic of overeating in restrained eaters (Herman and Mack 1975; Spencer and Fremouw 1979; Herman et al. This form of disinhibition or ‘the what the hell effect’ illustrates overeating in response to a high-calorie preload. Disinhibition in general has been defined as ‘eating more as a result of the loosening restraints in response to emotional distress, intoxication or preloading’ (Herman and Polivy 1989: 342), and its definition paved the way for a wealth of research examining the role of restraint in predicting overeating behaviour. The causes of overeating Research has explored possible mechanisms for the overeating shown by restrained eaters. These are described below and include the causal model of overeating, the boundary model of overeating, cognitive shifts, mood modification, denial, escape theory, overeating as relapse and the central role for control. They suggested that dieting and bingeing were causally linked and that ‘restraint not only precedes overeating but contributes to it causally’ (Polivy and Herman 1983). This suggests that attempting not to eat, paradoxically increases the probability of overeating; the specific behaviour dieters are Fig. The causal analysis of restraint represented a new approach to eating behaviour and the prediction that restraint actually caused overeating was an interesting reappraisal of the situation. Wardle further developed this analysis (Wardle 1980) and Wardle and Beales (1988) experimentally tested the causal analysis of over- eating. They randomly assigned 27 obese women to either a diet group, an exercise group or a no treatment control group for seven weeks. At weeks four and six all subjects took part in a laboratory session designed to assess their food intake. The results showed that subjects in the diet condition ate more than both the exercise and the control group supporting a causal link between dieting and overeating. From this analysis the overeat- ing shown by dieters is actually caused by attempts at dieting. According to the model, food intake is motivated by a physiologically determined hunger boundary and deterred by a physiologically determined satiety boundary. In addition, the boundary model suggests that the food intake of restrained eaters is regulated by a cognitively determined ‘diet boundary’. It indicates that dieters attempt to replace physiological control with cognitive control which represents ‘the dieters selected imposed quota for consumption on a given occasion’ (Herman and Polivy 1984: 149). Herman and Polivy (1984) described how after a low calorie preload the dieter can maintain her diet goal for the immediate future since food intake remains within the limits set by the ‘diet boundary’. The boundary model proposes a form of dual regulation, with food intake limited either by the diet boundary or the satiety boundary. The boundary model has also been used to examine differences between dieters, binge eaters, anorexics and normal eaters. Primarily this has been described in terms of a breakdown in the dieter’s self control reflecting a ‘motivational collapse’ and a state of giving in to the overpowering drives to eat (Polivy and Herman 1983). Ogden and Wardle (1991) analysed the cognitive set of the disinhibited dieter and suggested that such a collapse in self control reflected a passive model of overeating and that the ‘what the hell effect’ as described by Herman and Polivy (1984) contained elements of passivity in terms of factors such as ‘giving in’, ‘resignation’ and ‘passivity’. In particular, interviews with restrained and unrestrained eaters revealed that many restrained eaters reported passive cognitions after a high calorie preload including thoughts such as ‘I’m going to give into any urges I’ve got’ and ‘I can’t be bothered, it’s too much effort to stop eating’ (Ogden and Wardle 1991). In line with this model of overeating, Glynn and Ruderman (1986) developed the eating self-efficacy Fig. This also emphasized moti- vational collapse and suggested that overeating was a consequence of the failure of this self-control. An alternative model of overeating contended that overeating reflected an active decision to overeat and Ogden and Wardle (1991) argued that implicit within the ‘What the hell effect’ was an active reaction against the diet. This hypothesis was tested using a preload/taste test paradigm and cognitions were assessed using rating scales, interviews and the Stroop task which is a cognitive test of selective attention.

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