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ABSTRACT
What are the beliefs of adult patients on the prevention of adult obesity in primary care? A qualitative interview-based study Muhsanath M. Choudhury, BSc Medical Student, University College London m.choudhury@ucl.ac.uk doi:10.4201/lsjm.med.012 With: Dr Richard Meakin MD MSc FHEA (Clinical Senior Lecturer in General Practice), University College Medical School, London. Background: Obesity is an increasing problem for health care. Associated comorbidities are increasing with damaging effects on health and medical expenditure. The literature suggests the existence of weak interventions and identifies multiple barriers to obesity prevention.
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Aims & Objectives: This study aimed to explore patients’ beliefs on adult obesity prevention in order to better understand this problem and suggest prevention methods that are tailored to these beliefs. Methods: The study was a qualitative interview study using audio-taped semi-structured interviews. The interviews took place in an urban practice in North London where patients were recruited using posters and handouts. The subjects consisted of 14 adults, 7 male and 7 female with a wide range of characteristics (age, occupation, ethnicity and Body Mass Index). The collected data was analysed using the framework analysis technique.
dual-approach to personalised care through patient-centredness and doctor-direction leading to empowerment was preferred by patients. Comments: Few UK qualitative studies on patient beliefs regarding obesity prevention exist. This study uncovered beliefs, which may have a potential impact on medical education, clinical practice and health policy. Suggested interventions include, community activity programmes and group education settings held by GPs and other health professionals. The GP was seen as having the pivotal role as the main coordinator. These would address patient motivation and empowerment but the training of students and professionals would need to be addressed. Further research is indicated to further explore patients’ beliefs and to explore the views of GPs and other members of the primary care team involved in obesity prevention.
Results: Seven key themes emerged from the analysis which were: Time, Information, Awareness, Individuality, Getting Help, Understanding My Problem and Modern Living. Generally patients recognised a lack of public awareness and education as well as patient and doctor barriers affecting adherence to lifestyle change. Furthermore a
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ARTICLE
A discussion of drug-induced hyponatremia Tracey Liebman
Year 3 Medicine, New York University School of Medicine tracey.liebman@med.nyu.edu doi:10.4201/lsjm.med.011
Image: Wellcome Image
Diuretics Thiazides and loop diuretics have been implicated in association with hyponatremia. Thiazides have been shown to cause more cases of hyponatremia when compared to loop diuretics, though the mechanism not fully explained. Thiazides block the reabsorption of sodium and potassium at the distal convoluted tubule. Therefore, solutes are lost in the urine, and the ability to dilute the urine is diminished. Thiazides also lead to volume depletion, which is a stimulus for ADH release and can increase thirst. 2 Thiazides may also cause an idiosyncratic reaction that occurs rapidly and would therefore be more dangerous 1. Thiazides do not inhibit the ability of the kidney to concentrate urine, though loop diuretics interfere with concentration and
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dilution abilities. Thiazides were shown in one study by Liamis et al to be the most common cause of “community-developed hyponatremia�.2,2a The thiazide-induced hyponatremia has been seen often in elderly individuals.2,2a Individuals with low body mass and with hypokalemia are also at risk 1. In some studies, females have been shown to have a greater risk than males, but this has been controversial.1,2 Psychiatric medications Selective serotonin reuptake inhibitors and atypical antipsychotics may lead to SIADH and can cause hyponatremia. This possible complication is not common.3However; this can occur rapidly and therefore the harmful effects of acute hyponatremia may occur. There have been reports that all SSRIs can cause hyponatremia, but many of the studies are small and confounding factors abound. The hyponatremia soon is eliminated with removal of the drug; some studies have shown that it may be possible that patients may develop tolerance and that the hyponatremia effect could decrease. However, the overall risk of hyponatremia may be underestimated because cases may be asymptomatic In elderly patients who are taking SSRIs, the risk of hyponatremia is increased; for instance, the Swedish Adverse Drug Reactions Advisory Committee found that individuals over 70 years old had an increased risk.4 Patients should undergo fluid restriction and removal of the medication. Other classes of psychiatric drugs that may lead to hyponatremia include tricyclic antidepressants, monoamine oxidase inhibitors, nicotine, methadone, and benzodiazepines. However, the number of possible cases is extremely low. For example, in the literature there are fewer than 10 reported cases of hyponatremia associated with atypical antipsychotics.3 Antiepileptic medications Various antiepileptic medications have been associated with hyponatremia, as well. For instance, carbamazepine, oxcarbazepine, valproic acid, and lamotrigine have been implicated. In various studies, the rate of hyponatremia in patients treated with carbamazepine has ranged in 1.8% to 40% and with oxcarbazepine the rates have ranged from 23% to 73%.5 Many of these studies, as well, have been confounded by other factors that may increase the patient’s risk of hyponatremia such as increased age and other medications. The mechanism by which these antiepileptic drugs cause hyponatremia is not fully elucidated, but it may occur by increased reabsorption of water in the collecting tubule of the kidney.5 Many of these cases, as well, are asymptomatic and occur early in treatment.
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The cause of hyponatremia in a patient may be difficult to figure out, and the differential diagnosis can be complicated. Hyponatraemia, which is defined as serum sodium concentration less than 135 meq/L and is the most frequent electrolyte disorder in clinical practice, has a variety of etiologies, but can be caused by or complicated by the effect of medications.1 There are many categories of drugs that are associated with hyponatremia, including diuretics, psychiatric medications, antiepileptic drugs, and others.
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Others Chemotherapeutic agents such as vincristine, vinblastine, cyclophosphamide, cisplatin, and melphalan can stimulate the release of ADH and lead to hyponatremia.6
References
Angiotensin converting enzyme inhibitors, such as Lisinopril, have been described in very few cases in the literature to possibly be associated with severe hyponatremia. In these cases, the hyponatremia began after the ACE-inhibitor treatment was initiated, and it improved within days after the drug was stopped. The mechanism by which ACE-inhibitors are associated with hyponatremia is unclear, however, and some of these patients in the literature had also been taking other medications concurrently, so causality is difficult to prove.7, 8
3.
Omeprazole has been noted in case reports to be associated with SIADH and reversal of hyponatremia was noted when the drug was discontinued, but these findings are not well documented.9 Ecstacy (3,4-Methylenedioxymethamphetamine) may also lead to temporary increase in ADH along with ingestions of large quantities of water. This can bring about a symptomatic hyponatremia with symptoms such as confusion or coma and should be treated with water restriction.10 Conclusion A multitude of drugs can contribute in some way to SIADH and hyponatremia, and clinicians should not fail to consider these medications when evaluating a patient with complicated electrolyte disturbances.
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1.
2.
4. 5. 6. 7.
8.
9. 10.
Chow, K.M. et al. “Risk factors for thiazide-induced hyponatremia.” QJM. 2003 Dec; 96 (12) 911.2a. Liamis, G. “Blood pressure drug therapy and electrolyte disturbances.” Int J Clin Pract. 2008; 62(10):1572-1580. Liamis, G et al. “A Review of Drug-induced Hyponatremia.” Am J Kidney Dis. 2008; 52: 144-153. Kohen I et al. “Anti-Psychotic-induced hyponatremia: case report and literature review.” Am J Ther. 2008; Sep-Oct; 15(5): 492-4. Kirby, D and D Ames. “Hyponatremia and selective serotonin re-uptake inhibitors in elderly patients.” Intl J of Geriatr Psychiatry 2001; 16: 484-493. Castilla-Guerra L et al. “Electrolyte disturbances and Seizures.” Epilepsia. 2006; 47 (12) 1990-1998. Raftopoulos, Harry. “Diagnosis and management of hyponatremia in cancer patients.” Support Care Cancer. 2007; 14:1341-1347. Izzedine, Hassane et al. “Angiotensin-converting enzyme inhibitor-induced syndrome of inappropriate secretion of antidiuretic hormone: Case report and review of the literature.” Clin Pharm and Therapeutics. 2002 Jun;71(6):503-7. Hussain A Shaikh, Zakir. “Syndrome of Inappropriate Antidiuretic Hormone Secretion Associated with Lisinopril.” Annals of Pharmacotherapy. 2000; 34:176-9. Durst, Ronen Y et al. “Hyponatremia caused by omeprazole treatment.” Am J Med. 1994 Oct; 97 (4): 400-1. Farah, Raymond and Rola Farah. “Ecstasy-Induced Inappropriate Antidiuretic Hormone Secretion.” Pediatric Emergency Care. 2008; 24(9) 614-617.
11.
Other resources Fauci AS, Braunwald E, Kasper DL, SL Hauser SL, Longo DL, Jameson JL, Loscaizo J (eds), Harrison’s Principles of Internal Medicine, 17e. New York, McGraw-Hill, 2008. Milionis, Haralampos et al. “The hyponatremic patient: a systematic approach to laboratory diagnosis.” CMAJ 2002; 166 (8): 1056-62.
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REVIEW
Familial Hypercholesterolaemia Farwah Mehdi
ABSTRACT Background Those diagnosed with Familial Hypercholesterolaemia (FH) can improve their health by changing their behaviour. Health professionals should advise them to reduce fat intake, increase physical activity and stop smoking. A genetic test is available that can confirm the diagnosis of FH in those with high cholesterol. A potential concern is that this may undermine the likelihood of clinicians to give this advice and/or patients to follow it. Aims This cross-sectional interview study investigates: I. The ways in which clinicians giving genetic test results confirming a diagnosis of FH present the issue of behaviour change and II. Patients’ attitudes towards this advice and their motivation to make behavioural changes. Method The study sample comprised of seven FH patients who had received test results detecting the presence of a genetic mutation. These results were given to patients by a clinician during a specially arranged consultation. In-depth interviews were conducted with participants approximately one month after the results meeting, to achieve a better understanding of the impact of genetic testing on the thinking and behaviour of these individuals. Audio-recordings of the consultations and interviews were transcribed, anonymised and analyzed using both qualitative thematic and quantitative content analysis.
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Results Clinicians discussed the genetic cause of the condition and downplayed the role of behaviour and the desirability of behavioural changes: indications were made towards such changes being ineffectual in significantly reducing cholesterol levels. The emphasis was on medication as the most effective method in controlling cholesterol levels. Similarly, most patients were
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very confident about being able to adhere to medication and its efficacy in reducing cholesterol levels. However, patients also reported that they had made behavioural changes prior to genetic testing and were optimistic about attempting to maintain them. Conclusion Clinicians and patients appeared to have different models regarding behaviour change: patients recognised the value of lifestyle behaviour changes in combination with medication in managing FH, whereas clinicians emphasised the importance of medication. More research is needed to investigate ways in which clinicians could communicate with patients to encourage the adoption of lifestyle behaviour changes, as well as adhering to medication. Future research should explore the impact of genetic testing on the behaviour of those for whom genetic testing provided a new medical diagnosis, rather than, as in FH, confirming an existing one. INTRODUCTION Genetic testing is available for an increasing number of multifactorial conditions, which consist of a genetic component and are also influenced by the individual lifestyle choices that people make (Khoury et al., 2005; Yang et al., 2005). The rapid growth of this relatively new medical technology raises a variety of psychological and social issues that need to be addressed in order to appreciate its full potential. There are fears that the provision of personal genetic risk information will instigate a feeling of fatalism, with those tested experiencing diminished control over their condition and a reduced motivation to adopt risk reducing behaviour (Senior, Marteau and Peters, 1999; Marteau and Lerman, 2001; McClure, 2002; Haga, Khoury and Burke, 2003; Marteau and Weinman, 2006). A hypothetical study investigated the potential behavioural consequences of genetic testing for obesity risk. Participants assigned to a genetic high-risk group perceived to
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Medical Student, University College London farwah.mehdi@ucl.ac.uk doi:10.4201/lsjm.med.013
REVIEW
have less control over their behaviour than a genetic average risk group. However, there was no difference in the intention to eat a healthy diet between those given a high risk result based on a genetic test, and those given the same result determined via a hormone test (Frosch, Mello and Lerman, 2005). Another study of three hundred and forty-one families assessed the psychological impact of genetic testing to make or confirm a clinical diagnosis of FH, and found no support for the proposal that detection of a mutation precipitates fatalistic reactions. Results suggested that participants perceived biological methods used to control cholesterol levels to be more effective than behaviour changes, such as diet, owing to the genetic basis of the condition (Marteau et al., 2004). Some studies suggest that people are more likely to make healthier lifestyle changes subsequent to receiving personal genetic risk information (Audrain et al., 1997; McBride et al., 2002; Botkin et al., 2003; Schwartz et al., 2003). Patients from nine UK genetics centres that had undergone predictive genetic testing for breast and ovarian cancer predisposition by means of detecting mutations in the BRCA1 and BRCA2 genes, were asked to complete self-report questionnaires that considered the matter of risk management behaviour. Female gene mutation carriers were more inclined to embrace risk management strategies than non carriers in the year following the test. For example, ninety-two percent of carriers versus only thirty percent of noncarriers reported having had mammograms twelve months post-testing (Watson et al., 2004). Similarly, a recent analogue study recruited two hundred and sixty-one smokers who were randomly assigned to a scenario of having either a genetic or an oxidative test to assess heart disease risk. Results indicated that the genetic test-high risk group had a greater intent to quit smoking relative to the oxidative test-high risk group, which was partly due to a belief that smoking cessation would reduce chances of developing heart disease (Sanderson and Michie, 2007). Genetic testing is available for those affected by Familial Hypercholesterolaemia (FH) and, using cascade DNA testing, to aid in the accurate identification of family members that may also be affected (NICE CG71, 2008). FH is a dominantly inherited condition affecting one in five hundred of the general population but with a current detection rate of only 10% (Marks et al., 2004). Traditionally, the condition has been diagnosed clinically by the presence of elevated levels of low-density lipoprotein cholesterol (LDL-C), tendon xanthomata, premature onset of CHD and a family history of hypercholesterolaemia and premature CHD (Ward et al., 1996; Marteau et al., 2004). A number of mutations in the low-density lipoprotein receptor (LDL-R), apolipoprotein B (APOB) and PCSK 9 genes have now been robustly associated with FH (Austin et al., 2004). This knowledge has been used in the development of genetic testing as a method of confirming
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a clinical diagnosis in patients with FH (Marks et al., 2003), enabling those individuals to make behavioural changes to improve their long term prognosis (Marks et al., 2006). Where a LDLR/ APOB/PCSK 9 mutation is detected patients are advised to reduce dietary fat intake, take regular exercise, avoid smoking and adhere to prescribed lipid lowering medication (Betteridge et al., 1999). The aim of this project was to explore the impact of genetic testing on the health behaviour of FH patients and their relatives who have undergone genetic testing. A cross sectional interview study was conducted with patients recruited from a lipid clinic who had received a positive genetic test result, indicating the presence of a LDLR/APOB mutation. As part of the genetic service offered, participants attended a consultation in which a clinician communicated the test results. Specific research questions were: 1. How do clinicians present the issue of behaviour change? 2. What are the attitudes of participants towards behaviour change? 3. Does detection of an FH-causing mutation have an effect on motivation to make behavioural changes? The design of this study builds on prior studies since it investigated the way in which people talked about health behaviour, rather than using questionnaires with predetermined responses (Michie et al., 2003; Marteau et al., 2004). Much research has addressed similar questions in the context of other multifactorial conditions using an experimental analogue design and hypothetical scenarios (Frosch et al., 2005; Wright et al., 2008). This project was a real clinical situation with patients that had actually undergone DNA testing for FH, for which little qualitative work has previously been undertaken. To the author’s knowledge, there has been no previous work looking at the way clinicians communicate information regarding lifestyle behaviour changes, in the context of FH. However, this issue has been researched in primary care settings with family practitioners counselling patients to make lifestyle changes for both genetic and non-hereditary conditions (Arborelius, 1996; Arborelius and Bremberg, 1994). There is tentative evidence to suggest that clinicians may be less likely to use motivational strategies on patients with conditions believed to have a genetic cause (Thompson, Schwankovsky and Pitts, 1993). As well as adding to our understanding of patients’ reactions to a relatively new medical technology, the results of this project will be useful to health professionals in terms of communicating genetic information in a way that increases motivation to reduce risk. There may also be implications for the training of genetic
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REVIEW counsellors to increase their understanding of the psychological impact of the information they provide on their patients’ behaviour in relation to health. METHOD Design This is a cross-sectional interview study. Sample The recruitment of FH patients for DNA testing was ongoing as part of a three year DH-funded research arm of the UK FH Cascade Audit Project at the Royal Free Hospital. There were a total number of seven participants, who were FH patients that had received a positive DNA test result, (identification of a genetic mutation), to confirm the clinical diagnosis of the condition. The criteria for FH diagnosis are predefined (Betteridge et al., 1999), as are the methods for mutation detection (Heath et al., 2001). Participants are referred to by a number (e.g. III) to preserve anonymity. Procedure Approval from the NHS ethics committee was granted for this research project. Informed consent was obtained for samples to be taken from patients and sent to the DNA diagnostic laboratory at Great Ormond Street Hospital for analysis. A target of three months was set for returning the final test results of participants, on receipt of which, patients were invited to the Royal Free Clinic to be given their results by a clinician and arrange follow-up for family members. Consent was also obtained for the results consultation to be tape-recorded. During this meeting, patients were given a verbal introduction to the study by the Genetics Nurse, a further information sheet to read and an informed consent sheet to sign and return if they wished to participate. Those that agreed to take part in the study were contacted to arrange an interview approximately one month after receiving the test result, which were completed either in the patient’s home or in a special clinic visit, as preferred by participants. Qualitative, indepth interviews were conducted by the researcher of this project to gain an understanding of two general issues: communication of genetic information within a family and the impact of this information on the thinking and behaviour of individuals. The interviews were semi-structured and started with a schedule but important topics were probed as they arose. Both the interview and consultation for each of the seven participants were tape recorded, transcribed and anonymised, generating fourteen transcripts for analysis. Analysis The interview and consultation transcripts for each of the seven FH patients were read and re-read individually by the author to identify and extract quotations relating to: 1. 2. 3.
The way clinicians presented the issue of behaviour change. The attitudes expressed by patients towards behaviour change. Responses given by patients regarding their motivation to make behaviour changes.
This process entailed considering both lifestyle behaviour changes (e.g. diet, physical activity, smoking and cholesterol checks) and
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medication use but as two separate categories. A word search was then carried out for each transcript using the Microsoft Word package to ensure that all relevant quotations had been gathered. Words that were used included: pills, tablets, medicine, medication, statins, drugs, prescription, treatment, diet, fat, oil, sugar, alcohol, food, weight, healthy, habit, intake, drink, eat, physical, activity, exercise, gym, sport, walk, fit, active, smoke, cigarettes, check, test, level, precautions and cautious. One consultation and one interview transcript containing a high frequency of quotations, as deemed by the author, were emailed to the researcher involved in the project to read, and similarly extract relevant passages of the transcripts. A comparison was then made to check whether the researcher and author had identified the same quotations. Qualitative thematic analysis (Joffe and Yardley, 2004) was carried out for each participant individually, using the quotations separated from both consultation and interview transcripts. Emergent themes for each patient, together with the illustrative quotations, were emailed to the principal investigator of the project to be checked and refined. These themes were then compared across all participants and used to devise a coding frame to identify and categorize the parts of the transcripts that addressed the specific research questions of this study. The frequencies of illustrative quotations for each theme were recorded, with totals, averages and ranges subsequently being calculated to give a quantitative content analysis. In addition, the number of lines of interview and consultation transcripts and, therefore, percentage of total transcript that referred to behaviour was worked out for both patients and clinicians. All figures were calculated to one decimal place. By convention, all elisions in the text will be indicated by three dots, with square brackets used for insertions or clarifications made by the author. (Green and Thorogood, 2004, pg. 101). All quotations are labelled as follows: (VII, C/I, pg 3, 115-117). This information translates to the participant number, source of the quotation; where ‘C’ represents the consultation transcript and ‘I’ the interview transcript, page number and line numbers. ‘C’, ‘P’ and ‘I’ are the abbreviations used to indicate whether the quotations belong to the clinician, participant or interviewer respectively. Results References to four different behaviours were made across interviews conducted with the seven participants: diet, physical activity, monitoring cholesterol levels via regular tests or appointments and medication. Additionally, participants I and III mentioned that they had given up smoking during consultations with the clinician but not when interviewed: And then I stopped smoking (III, C, pg 2, 70) In the past I was, I have been, I have, I smoked for, and I have given it up from 18 years. In 1989, I think, as far as I remember, I gave it up. I was smoking earlier. (I, C, pg 8, 339-241) The range of references made to behaviour over individuals was ten, and for across all four behaviours was sixteen. Table 2 indicates that references were made to medication and diet by
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REVIEW Table 1: Demographic characteristics of participants recruited in study Participant Number I II III IV V VI VII
Gender
Age (Years)
Male Female Female Female Female Female Male
Nationality
77 64 Unknown 75 75 29 46
Ethnic Group
Iraqi British British British British Kosovan Turkish
Non-White White White White White Non-White Non-White
Table 2: Frequency of references made to behaviour by participants during interviews Participant Number I II III IV V VI VII
Diet 3 3 4 2 1 4 3 20 2.9
Total Average number of references per participant Range of references made between each behaviour
Physical activity 0 0 3 0 1 2 1 7 1.0
3
3
Cholesterol tests and appointments 1 3 1 2 0 3 2 12 1.7
3
Medication 1 4 6 5 1 2 4 23 3.3
Total 5 10 14 9 4 11 10 62 8.9
5
Table 3: Percentage of total interview transcript that referred to behaviour (diet, physical activity, cholesterol tests/appointments and medication) for participants Participant Number
I II III IV V VI VII Average From table 3 and 4 it is evident that the issue of health behaviour comprised of less than 10% of the interview and consultation transcripts. However, the percentage of total interview transcript that referred to health behaviour was almost double that of the consultation transcript. How do clinicians present the issue of behaviour change? Three categories were derived from the ways in which the clinician related the matter of lifestyle behaviour changes to participants
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Number of lines of transcript referring to behaviour 28 82 46 62 13 58 46
Percentage of interview transcript referring to behaviour (%) 3.0 7.1 5.6 6.7 1.8 7.2 3.7 5.0
across all seven consultations, as illustrated in table 5. The clinician commenced five of the consultations in a similar manner by mentioning that a link existed between different lifestyle choices made by individuals and cholesterol levels: *Um, so there’re lots of reasons why people can have raised cholesterol other than genetic reasons, just from diet, eating the sort of fat in the diet, and not taking enough exercise. (III, C, pg 1, 17-19)
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REVIEW Table 4: Percentage of total consultation transcript that referred to behaviour (diet, physical activity, cholesterol tests/appointments, smoking and medication) for clinicians Participant number
Number of lines of transcript referring to behaviour
I II III IV V VI VII
36 11 83 20 9 9 3
Average
Percentage of consultation transcript referring to behaviour (%) 3.1 1.3 6.5 2.0 1.4 2.2 1.5 2.6
Table 5: Categorization of the ways clinicians presented lifestyle behaviour changes to participants Participant number
I II III IV V VI VII Total
Instances that clinician downplayed lifestyle behaviour change in context of genetic cause and/or medication 2 1 1 1 1 0 1 7
Instances that a link between behaviour change and cholesterol was mentioned
Total
3 0 4 0 0 0 0 7
1 1 1 0 1 1 0 5
7 2 6 1 2 1 1 19
Clinicians downplayed lifestyle behaviour changes in six out of seven consultations by placing less emphasis on the potential efficacy of such changes in reducing cholesterol levels. Only in the cases of participants I and III did the clinician advise on the utility of some lifestyle behaviour changes, however others were simultaneously downplayed, thus providing these two patients with conflicting advice regarding the overall benefit of lifestyle behaviour changes. For example, during the consultation with participant III, physical activity was encouraged whilst diet was downplayed in the context of the genetic cause of FH by the clinician:
that doesn’t have that much effect on the problem. (III, C, pg 2, 61-68)
P: I do take a lot of exercise… I just walk everywhere… so I do do a lot of walking actually…I love it, even in the winter, it doesn’t matter - you know what I mean? C: ... it’s helping your cholesterol as well (III, C, pg 1, 21-50)
a) b)
P: I do eat very healthily…I don’t eat chips and I don’t eat takeaways, and I cook everything myself, and I do eat fruits, but you know, so I’m doing my best and there’s nothing more, really, I can do about it. C: Yeah, that sounds perfect, so for someone who doesn’t have a genetic cause, then doing all that can help, but if you’ve got FH all
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Instances that clinician positively promoted lifestyle behaviour change
The effectiveness of medication was always reinforced by the clinician when broached in five of the consultations, as discerned from table 6. Likewise, all seven participants showed evidence of adhering to the prescribed statins and no predicaments were reported in implementing this behaviour change. The attitudes identified from analysis of the transcripts were broadly divided into those in which patients: Felt positive about carrying out behaviour changes and/or expressed a belief that these were effective in controlling cholesterol levels. Felt pessimistic about the potential value of behaviour changes and/or held the view that these were not effective in reducing cholesterol levels.
As observed from table 7 and 8, the total frequency of statements made by patients that reflected a feeling of control with respect to behaviour change was higher than those that alluded towards a perceived lack of control. A greater number of attitudes expressing confidence in medication as opposed to lifestyle
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REVIEW behaviour changes were also recorded. Participants II, III, IV and VI all believed that medication effectively reduced their cholesterol levels. In the instances that participants I and III exhibited a degree of pessimism and loss of confidence in medication and diet, it was noted that this was not accompanied by a reduced motivation to adhere to those particular changes. Motivation to make behaviour changes Two of the participants revealed that genetic testing had impacted on their motivation to make behavioural changes, as shown in table 9. Participant VII exhibited a greater inclination to increase his physical activity levels, whilst participant VI indicated that her diet had become less rigid as a result of testing positive for a genetic mutation. In the case of the latter, this was owing to an attribution of the condition to genes and a belief that diet no longer had a causal influence on cholesterol levels. Referring back to table 5, it can be seen that the clinician only mentioned the presence of a link between cholesterol and behaviour change during the consultation with participant VI, and in fact downplayed behaviour change in the meeting with participant VII. Participants I, II, III and IV demonstrated efforts to try and persevere with lifestyle behavioural changes made prior to testing, and showed an awareness of the different approaches used in managing cholesterol levels.
value of any previous encouragement given. Medication use was positively promoted when mentioned during consultations and emphasis placed on this biological based way being more effective than any behavioural changes made to lifestyle. There was no evidence of feelings of fatalism as a result of receiving a positive genetic test result, with most participants conveying optimism and confidence in maintaining risk-reducing behaviour. The patients who did express a degree of pessimism did not completely withdraw from engaging in those particular behaviours but showed attempts to comply with the approaches used in treating FH. These results can be considered in the context of Leventhal’s common sense model of self-regulation of health and illness, which describes the way health risk information evokes cognitive representations of the threat in people based on five dimensions: identity, cause, timeline, consequences and control (Cameron and Leventhal, 2003). This is used as guidance in determining which strategies should be drawn upon in order to control the threat. The outcomes are then appraised and used to feed back to their appraisals of threat and coping. Patients in this study were previously aware and being treated for their clinical diagnosis of FH, and so had experience of methods effective in controlling cholesterol levels, by undergoing continual evaluations to ascertain which behaviours to pursue and maintain. Therefore, the threat posed by FH was perceived as being a controllable one by most participants. (Marteau and Weinman, 2006).
Three models emerged with respect to the utility of lifestyle behaviour changes, as illustrated by the quotations in tables 10 a), b) and c):
Confirmation of a clinical diagnosis of FH via genetic testing did not appear to alter the overall motivation of patients to make behavioural changes in relation to health. Most participants 1. Due to genetic cause of FH and/or because the patient continued to apply the same management techniques to control is taking medication, lifestyle behaviour changes do not cholesterol levels that were being used prior to testing positive make much difference. for a mutation; namely a combination of adhering to prescribed 2. Lifestyle behaviour changes are important. medication and attempting to be more cautious with their diets. 3. Lifestyle behaviour changes work in combination with This is consistent with a previous randomized controlled trial in medication. which there was no difference in the total fat intake, frequency of vigorous exercise, self reported rates of smokers and number of Clinicians and patients did not share the same models, since in participants taking statins amongst those with a genetic diagnosis most cases clinicians demonstrated a belief that lifestyle behaviour of FH and those with just a clinical diagnosis for the condition changes made no difference to cholesterol levels due to the (Marteau et al., 2004). Similarly, there was no significant genetic basis of FH and/or in the context of medication. However, difference in the levels of attendance for mammography in females most of the participants recognized the importance of making before and after receiving genetic test results that revealed an behavioural changes in addition to medication use. increased predisposition to inheriting breast cancer (Lerman et al., 2000). A further study, of analogue design, found that genetic DISCUSSION risk information did not encourage adults to engage in riskIn this study, clinicians predominantly downplayed lifestyle reducing behaviour to a greater extent than receiving family-history behaviour changes by indicating that such changes were ineffective based risk information (Hicken and Tucker, 2002). A speculative in reducing cholesterol levels due to the genetic cause of FH. explanation in the context of this project is that people strive to Comparisons were also made to the beneficial impact lifestyle perceive their world as being stable, predictable and controllable behaviour changes had in those individuals with high cholesterol by contriving causal explanations for events (Heider, 1958). Hence, levels that were not under the influence of a genetic component. holding the view that FH is influenced by both genes and lifestyle This provides support for the suggestion that physicians are enables an increased perception of control (Senior et al., 2002). less likely to use motivational strategies in case presentations The one participant that did reveal a reduced adherence to diet of hereditary conditions (Thompson, Schwankovsky and Pitts, after receiving the genetic test results attributed her condition 1993). Patients were not advised to make lifestyle behavioural solely to genes and rejected the idea of diet having an effect on her changes in any of the consultations. However, when patients cholesterol levels. This may have reduced the patient’s perception initiated discussion regarding the utilisation of different techniques of control over FH and so weakened her will to maintain a to manage FH, clinicians praised and advocated their efforts in restrictive diet. Although variation was observed across participants attempting to lower cholesterol levels. In these instances, other regarding their views on the relative effectiveness of different lifestyle behavioural changes were simultaneously downplayed risk-reducing behaviours, no-one reported FH treatment to be by the clinician, which may have reduced the overall benefit and completely ineffectual (Senior, Marteau and Weinman, 2005).
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REVIEW All participants exhibited adherence to prescribed statins and this was generally regarded as an effective means of controlling cholesterol levels, with no concerns reported in implementing this behaviour. The study by Marteau and colleagues (2004), also investigating the psychological impact of genetic testing for FH, suggested that on receiving results testing positive for a mutation, patients altered their perceptions of the way in which control of cholesterol levels was best elicited. Learning of the genetic basis of the condition reinforced biological methods of control (e.g. medication) versus behavioural changes, principally dietary interventions. This is also supported by an analogue experimental study that explored smoking cessation in smokers who were given the hypothetical situation of testing positive for a genetic predisposition to nicotine dependence. Participants were more likely to opt for pharmacological methods to aid in quitting smoking and less likely to use willpower. Overall perceptions of control were not significantly different between gene positive and gene negative individuals (Wright, Weinman and Marteau, 2003). The current study cannot provide further support for this hypothesis, since although FH patients did show confidence in the value of statins, lifestyle behavioural changes were not simultaneously downplayed by all participants.
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Overall, clinicians and patients did not hold the same models with respect to behaviour changes. Whereas clinicians reinforced cholesterol-lowering medication as the best way to treat FH, patients adopted a multifactorial approach: taking medication in combination with attempting to adhere to lifestyle behaviour changes. Following genetic counselling, patients use beliefs about inheritance, personal and family experience to regenerate their risk perceptions (Emery, Kumar and Smith, 1998; Peters and Biesecker, 1997). A study demonstrated that only 9% of relatives of Cystic Fibrosis patients obtained knowledge of the disease from a genetic counsellor, with the rest being accessed from family members and family doctors (Denayer et al., 1992). It was found that people perform correctly on knowledge tests about the condition but convey beliefs and understandings that differ from this knowledge (Weil, 1991; Shiloh, 2006). This may explain the findings in relation to participant VI, who had an increased motivation to increase physical activity levels despite the clinician downplaying this behaviour change during her results meeting. The ethnic group of the patient may have had a bearing on health behaviour and the attitudes expressed towards FH. There is evidence to suggest that cultural, ethnic and religious factors are accounted for when individuals interpret genetic information (Richards, 1996; Wilson et al., 2004). These factors may incite discordance between professional and lay theories, resulting in reluctance on the patient’s part to endorse the advice given by clinicians (Browner et al., 2003; Shiloh, 2006). Caution should be taken in making generalizations from this study since it comprised of a small sample, was drawn from one lipid clinic and patients were tested for one condition. The fact that the patients already had a clinical diagnosis of FH, were taking medication, regularly attending the lipid clinic, and agreed to take part in the study means that the genetic test results probably had less of an impact on behaviour than on those individuals previously unaware of a diagnosis of FH. In addition, most patients were over sixty years of age and so had previous experience of dealing with the condition. An earlier study also found that older patients are
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more likely to report total adherence to behaviours in treating FH (Senior et al., 2002). The cognitive representations formed by individuals in response to health risk information are dynamic and change over time, thus the attitudes and beliefs captured during the interview, which was held one month after receiving the test results may be subject to change (Hallowell and Richards, 1997) The main implication of this project concerns effective communication with patients about the benefits of lifestyle behaviour changes, even when a condition is attributed to a genetic cause. A patient-centred approach should be used to gauge an appreciation of the patient’s own unique beliefs, understanding and social environment to facilitate in empowering individuals to make behaviour changes (Lynch and Lynch, 1996). Studies researching the effect of ethnic group on health behaviour are required to ensure genetic services facilitate informed decision-making in the cosmopolitan environment of the UK. Future research should explore whether the same results are obtained in a population previously unaware of the possible diagnosis, such as relatives who have tested positive for a genetic mutation. Further work is also needed to investigate ways of communicating with these patients in order to encourage their engagement with healthy lifestyle behaviour changes, in addition to adhering to their medication regime. Acknowledgements I am very grateful to Susan Michie for all her support, guidance, helpful comments and suggestions and to Caroline Dancyger for the all the data collection of this project.
References 1. 2. 3. 4. 5. 6. 7. 8.
Arborelius E and Bremberg S. (1994). Prevention in practice. How do general practitioners discuss life-style issues with their patients? Patient Education and Counseling. 23, 23-31 Arborelius E. (1996). Using doctor-patient communication to affect patients’ lifestyles. theoretical and practical implications. Psychology and Health. 11 (6), 845-855. Audrain J, Boyd NR, Roth J, Main D, Caporaso NF and Lerman C. (1997). Genetic susceptibility testing in smoking- cessation treatment: one-year outcomes of a randomized control trial. Addictive behaviors. 22(6), 741-751 Austin MA, Hutter CM, Zimmern RL and Humphries SE. (2004). Genetic causes of monogenic heterozygous Familial Hypercholesterolaemia: a HuGE prevalence review. American Journal of Epidemiology. 160(5), 407-420. Betteridge DJ, Broome K, Durrington PN, Hawkins MM, Humphries SE, Mann JI, Milller JP, Neil HAW, Thompson GR and Thorogood M. (1999). Scientific steering committee on behalf of the Simon Broome Regisetr Group. Mortality in treated heterozygous familial hypercholesterolaemia: implications for clinical management. Atherosclerosis. 142, 105-112. Botkin JR, Smith KR, Croyle RT, Baty BJ, Wylie JE, Dutson D, Chan A, Hamann HA, Lerman C, McDonald J, Venne V, Ward JH and Lyon E. (2003). Genetic testing for BRCA1 mutation: Prophylactic surgery and screening behaviour in women 2 years post testing. American Journal of Medical Genetics. 118, 201-209. Browner CH, Preloran HM, Casado MC, Bass HN and Walker AP. (2003). Genetic counseling gone awry: miscommunication between prenatal genetic service providers and Mexican-origin clients. Social Science and Medicine. 56 (9), 1933–1946. Cameron LD, Leventhal H. (Eds.) (2003). The Self-Regulation of Health and Illness Behaviour . London : Routledge.
lsjm 30 april 2010 volume 01
ABSTRACT
The media and medical response to the introduction of prescription charging in the National Health Service Louis John Koizia
Keywords: • NHS • Prescription • BMA
Image: Wellcome Image
Year 5 Medicine, Imperial College London louis.koizia05@imperial.ac.uk
Abstract: In April 2009 the National Health Service (NHS) prescription charge rose to £7.20 in England, whereas in Wales prescriptions have been free since 2007. This major difference has led to much controversy amongst the public, media and medical profession. When established on July 5th 1948 the NHS provided free healthcare including prescriptions to the entire population of Britain. However, concerns arose shortly after establishment, when in 1949 the expenditure of the NHS was far in excess of the initial estimate; By June 1952 the Conservative government introduced a one shilling prescription charge. Previous literature has focused on the political debate which surrounded this charge. The purpose of this paper is to historically assess the response from the media and the medical profession. Information gathered from the newspapers, despite their differing readerships and political affiliations, revealed that the media generally accepted the charge with little opposition. In contrast, large debate and divisions arose amongst the medical profession, with huge volumes of literature being published in medical journals throughout 1952 on the issue. The London based British Medical Association opposed the charge as they felt doctors were not government tax collectors; whereas rural doctors became concerned that the charge would affect the doctor-patient relationship. This paper identifies that the introduction of the prescription charge, not only aroused debate in parliament, but caused a spectrum of views amongst lay and medical circles.
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