Issues

Volume 164 Issue 3

5 February 1996

Editorials Hepatitis C: questions to be answered Simone I Strasser 132That's the limit: alcohol consumption and health John B Saunders 133Oily fish and asthma - a fishy story? Francis C K Thien, Rosalie K Woods, E Haydn Walters 135 Research Consumption of oily fish and childhood asthma risk Linda Hodge, Cheryl M Salome, Jennifer K Peat, Michelle M Haby, Wei Xuan, Ann J Woolcock 137Meta-analysis of alcohol and all-cause mortality: a validation of NHMRC recommendations C D'Arcy J Holman, Dallas R English, Elizabeth Milne, Michael G Winter 141Acute rheumatic fever and rheumatic heart disease in the Top End of Australia's Northern Territory Jonathan R Carapetis, Don R Wolff, Bart J Currie 146Chronic hepatitis C and interferon alfa therapy: predictors of long term response Peter J Jenkins, Suzanne L Cromie, D Scott Bowden, Caroline F Finch, Francis J Dudley 150 Notable Cases When is hypospadias not hypospadias? Steven Y C Tong, Karen Donaldson, John M Hutson 153 Review Working overseas: obtaining a residency or fellowship in the United States Martin J Carey, Therese M Dawson, Kim M Yates 155 Viewpoint Caring for a vulnerable population Helen P Beange 159 Managing HIV Structure and function of HIV Anthony L Cunningham, Dominic E Dwyer, John Mills, Luc Montagnier 161How HIV produces immune deficiency Rosemary Ffrench, Graeme J Stewart, Ronald Penny, Jay A Levy 166How HIV leads to opportunistic infections Suzanne M Crowe, Richard S Kornbluth 171 Medicine and the Community Great expectations: the coroner's report on the South Australian haemolytic uraemic syndrome outbreak Craig B Dalton, Robert M Douglas 175 Medicine and the Law Is there a medical litigation crisis? Paul A Komesaroff, Megan A Keaney, Paul Nisselle, Ian M Dunn 178

Editorials

Immune system diseases 5 February 1996 Free

Oily fish and asthma - a fishy story

Editorial Oily fish and asthma - a fishy story? Further studies are required before claims can be made of a beneficial effect of oily fish consumption on asthma Interest in the possible health benefits of dietary fish lipids followed observations that populations with a high dietary intake of fish, such as Greenland Inuit and the Japanese, had low incidences of atherosclerotic disorders and of inflammatory conditions such as rheumatoid arthritis. Our recent understanding of asthma as a chronic inflammatory airway disease has led to speculation that a diet rich in fish oil may also ameliorate asthma. The potential anti-inflammatory effect of fish oil stems from its active ingredient, eicosapentaenoic acid (EPA), which is a competitive substrate with arachidonic acid for the generation of inflammatory mediators. The derivatives of arachidonic acid (an n-6 fatty acid) are leukotriene B4 (LTB4), a potent neutrophil chemoattractant and pro- inflammatory mediator, and the cysteinyl series of leukotrienes (LTC4, LTD4 and LTE4), which produce potent smooth muscle contraction and bronchoconstriction. In contrast, EPA (an n-3 fatty acid), as well as inhibiting arachidonic acid metabolism, is a substrate for the less active prostanoids (e.g., thromboxane A3) and leukotrienes (e.g., LTB5), and so has the potential to reduce airway inflammation and reverse bronchoconstriction. As the most profound anti-inflammatory actions of fish oil are on neutrophil function and mediator generation, it is not surprising that clinical trials of dietary fish oil have been beneficial in diseases where there is a neutrophilic inflammation, such as rheumatoid arthritis, psoriasis, cystic fibrosis and inflammatory bowel disease. However, in asthma the role of neutrophils is much less certain. Eosinophils and mast cells are thought to be the predominant effector cells in asthma (through the release of mediators), with T lymphocytes, macrophages and, possibly, mast cells having initiating and immunomodulatory roles through cytokine secretion. Placebo-controlled interventional studies of high dose fish oil supplementation in patients with asthma have been disappointing. Early short term trials (eight weeks) of up to 4 g/day of EPA in severe asthmatics showed no clinical benefit, despite demonstrating profound suppression of neutrophil chemotaxis and mediator generation.1 In a study in aspirin-intolerant subjects asthma control worsened after six weeks of 3 g/day of EPA, 2 consistent with the known aspirin-like effect of cyclooxygenase inhibition by EPA. Further studies in milder asthmatics with 3.2 g/day for 10 weeks showed no benefit in either clinical symptoms or bronchial hyperresponsiveness,3 despite demonstrating attenuation of allergen-induced late-phase bronchoconstriction induced in the laboratory.4 A more prolonged trial for six months with 3.2 g/day of EPA also showed no clinical benefit in patients with pollen-induced asthma and seasonal hayfever.5 These disappointing results are consistent with in-vitro evidence that EPA does not inhibit eosinophils and mast cells. In contrast to its dampening effect on neutrophils, EPA incubated with cultured murine mast cells produced a marked increase in production of platelet-activating factor, without an effect on histamine release.6 Similarly, stimulated human eosinophils incubated with EPA generated significantly greater amounts of leukotrienes than those incubated with arachidonic acid.7 Furthermore, in asthma there is a complex interaction between cells, cytokines, nerves and lipid and other mediators. Although of the lipid mediators leukotrienes may have the most influential role in asthma, modulating any one group of inflammatory mediators alone may not be sufficient to produce clinical improvement. The only interventional study which has shown positive results was a small placebo-controlled trial of low-dose EPA (1 g/day) for 12 months in 12 adult asthmatic subjects (six taking fish oil and six taking placebo). After nine months a small but significant improvement was found in forced expiratory volume at one second (FEV1).8 However, no details were given of concurrent medication use or assessment of compliance with therapy by leukocyte membrane phospholipid analysis, and there have been no follow-up data since 1991. The question of fish diet and respiratory health has also been investigated from an epidemiological perspective in recent American studies. In a survey of 2526 adult subjects aged 30-70 years, the first National Health and Nutrition Survey found eating fish more than once a week, compared with less than once a week, was associated with a higher level of lung function. However, only 2.9% of subjects in this survey were asthmatic, so no conclusion could be drawn about the effect of fish consumption on asthma.9 The Atherosclerosis Risk in Communities (ARIC) study surveyed 8960 adult current and former smokers10 and reported that a high dietary intake of n-3 fatty acids was inversely related to the risk of chronic obstructive pulmonary disease (COPD). This apparent protective effect is biologically plausible as neutrophilic inflammation is a feature of COPD. The Nurses' Health Study, possibly the largest prospective study of its type, reporting the incidence of adult-onset asthma in 77 866 women aged 34-68 years, found no relationship between dietary intake of fatty acids and the incidence of doctor-diagnosed asthma over a 10-year period.11 With this background, what interpretation can be put on the study by Hodge et al. in this issue of the Journal (page 137)? The novel aspects of this epidemiological survey are that the study population consisted of Australian children aged 8-11, and that the diagnosis of asthma was based both on symptoms and measurement of bronchial hyperresponsiveness. The investigators found an inverse relationship between weekly oily fish intake and prevalence of asthma in 574 schoolchildren. A number of salient points may be made. Firstly, the investigators previously reported an inverse relationship between weekly total fish intake and asthma, which is not evident in this study. This may reflect the inherent variability of food frequency questionnaire data or the different sample sizes of the two studies, but it does raise doubts about the primary hypothesis being tested. Secondly, the estimated mean intake of EPA from a weekly serve of fish10 is about 0.2-0.8 g, which is much lower than the amount that would be expected to have anti-inflammatory effects on leukocyte mediator and cytokine generation. It is possible that it is not the oil in the fish per se but some other dietary or social component associated with families who eat fish which is responsible for these results. Thirdly, a much larger prospective study in adults did not find a similar relationship between dietary fish intake and asthma prevalence.11 Can this discrepancy be explained by subtle effects of low-dose fish oil on the immunological development of asthma in childhood, which are no longer relevant in adulthood? There is currently insufficient understanding of the mechanisms involved to put forward a biologically plausible hypothesis. Finally, the study of Hodge et al. is a cross-sectional study, and thus cannot establish a temporal relationship between oily fish intake and asthma. Nevertheless, these are very interesting data but they need to be confirmed in larger studies. Placebo-controlled prospective intervention studies with dietary manipulation for prolonged periods in childhood are also required before any claim can be substantiated. Until then, unwarranted speculation about the relationship between dietary fats and asthma12 should be avoided as this may have a negative impact on other health outcomes, cause even more confusion about diet and health in the general population and undermine an evidence-based approach to public health initiatives. Francis C K Thien Senior Lecturer Rosalie K Woods Research Fellow E Haydn WaltersProfessor/Director Department of Respiratory Medicine, Alfred Healthcare Group Melbourne, VIC (©MJA 1996; 164: 135-136) Kirsch CM, Payan DG, Wong MYS, et al. Effect of eicosapentaenoic acid in asthma. Clin Allergy 1988; 18: 177-187. Picado C, Castillo JA, Schinca N, et al. Effects of a fish oil enriched diet on aspirin intolerant asthmatic patients: a pilot study. Thorax 1988; 43: 93-97. Arm JP, Horton CE, Mencia-Huerta J-M, et al. Effect of dietary supplementation with fish oil lipids on mild asthma. Thorax 1988; 43: 84-92. Arm JP, Horton CE, Spur BW, et al. The effects of dietary supplementation with fish oil lipids on the airways response to inhaled allergen in bronchial asthma. Am Rev Respir Dis 1989; 139: 1395-1400. Thien FCK, Mencia-Huerta J-M, Lee TH. Dietary fish oil effects on seasonal hay fever and asthma in pollen-sensitive subjects. Am Rev Respir Dis 1993; 147: 1138-1143. Triggiani M, Connell TR, Chilton FH. Evidence that increasing the cellular content of eicosapentaenoic acid does not reduce the biosynthesis of platelet-activating factor. J Immunol 1990; 145: 2241-2248. Thien FCK, Hallsworth MP, Soh C, Lee TH. Effects of exogenous eicosapentaenoic acid on generation of leukotriene C4 and leukotriene C5 by calcium ionophore-activated human eosinophils in vitro. J Immunol 1993; 150: 3546-3552. Dry J, Vincent D. Effect of a fish oil diet on asthma: results of a 1-year double-blind study. Int Arch Allergy Appl Immunol 1991; 95: 156-157. Schwartz J, Weiss ST. The relationship of dietary fish intake to level of pulmonary function in the first National Health and Nutrition Survey (NHANES I). Eur Resp J 1994; 7: 1821-1824. Shahar E, Folsom AR, Melnick SL, et al. Dietary n-3 polyunsaturated fatty acids and smoking-related chronic obstructive pulmonary disease. N Engl J Med 1994; 331: 228-233. Troisi RJ, Willett WC, Weiss ST, et al. A prospective study of diet and adult-onset asthma. Am J Respir Crit Care Med 1995; 151: 1401-1408. Hodge L, Peat JK, Salome C. Increased consumption of polyunsaturated oils may be a cause of increased prevalence of childhood asthma. Aust N Z J Med 1994; 24: 727. (©MJA 1996; 164: 135-136)

Rosalie K Woods

Research

Immune system diseases 5 February 1996 Free

Consumption of oily fish and childhood asthma risk

Research Consumption of oily fish and childhood asthma risk Linda Hodge, Cheryl M Salome, Jennifer K Peat, Michelle M Haby, Wei Xuan and Ann J Woolcock For editorial comment, see Thien et al. Abstract - Authors' details - Introduction - Methods - Results - Discussion - Appendix - Acknowledgements - References - Box 1 - Box 2 - Box 3 - Figure - © MJA 1996 - Abstract Objective: To investigate the association between diet and airway disease in children in the light of epidemiological studies suggesting that consumption of fish more than once a week reduces the risk of developing airway hyperresponsiveness (AHR). Design: Diet was assessed by a detailed food frequency questionnaire and airway disease by respiratory symptoms or airway responsiveness to exercise. Methods: A questionnaire, containing questions about the frequency of eating more than 200 foods, was sent to the parents of 574 children in whom we had measured recent wheeze (by questionnaire), AHR (by exercise) and atopy (by skin prick tests) six months before this study. We defined current asthma as the presence of both recent wheeze and AHR. Results: Response rate to the questionnaire was 81.5% (n = 468). After adjusting for confounders such as sex, ethnicity, country of birth, atopy, respiratory infection in the first two years of life and a parental history of asthma or smoking, children who ate fresh, oily fish (> 2% fat) had a significantly reduced risk of current asthma (odds ratio, 0.26; 95% confidence interval, 0.09-0.72; P < 0.01). No other food groups or nutrients were significantly associated with either an increased or reduced risk of current asthma. Conclusion: These data suggest that consumption of oily fish may protect against asthma in childhood. MJA 1996; 164: 137-140 Introduction The substantial increase in the prevalence of childhood asthma in the past 20 years has affected both rural and urban communities of westernised countries,1,2 suggesting that local environmental factors, such as exposure to allergens or industrial air pollutants, are not the cause. However, the widespread changes in diet may be responsible. Seaton et al.3 have postulated that increases in the prevalence of asthma may be due to a reduced intake of antioxidant vitamins (beta-carotene, vitamins A, C and E) and mineral cofactors essential for antioxidant defence mechanisms (selenium, zinc and copper) as a result of reduced consumption of meat, fresh fish, fruit and vegetables in Western diets. Reduced consumption of magnesium4 and increased consumption of salt5 have been implicated as risk factors for airway hyperresponsiveness (AHR). Our own epidemiological studies of Australian schoolchildren have shown that children who eat fish more than once a week have a third the risk of AHR of children who do not eat fish regularly.6 However, these studies did not include other dietary questions, so that fish consumption may have been a marker for another dietary characteristic. Here, we investigate the association between diet, as assessed by a detailed dietary questionnaire, and airway disease, assessed by respiratory symptoms or airway responsiveness to exercise. Methods Subjects In June 1993, a cross-section of 808 children aged 8-11 years from schools randomly selected from all schools within a 10 km radius of Sydney General Post Office had airway responsiveness to exercise, respiratory symptoms and atopy measured and frequency of fish consumption assessed.7 In October 1993, 584 children were selected from this group in a stratified case-control design and their parents were asked to complete a detailed food frequency questionnaire about their child's eating habits. The selection criteria included all children with AHR, all children who had had wheeze in the last 12 months (recent wheeze) and a three-in-five sample of children with normal airways (no AHR or recent wheeze), who were chosen by excluding two children after every three from numerically ordered lists of children identified by number. The study coordinator who collected the food frequency questionnaires was blind to the respiratory symptom and AHR status of the subjects. Ethical approval for the study was obtained from the Ethics Review Committee of the University of Sydney. Permission to approach schools was obtained from the New South Wales Department of School Education and the Catholic Education Office. Respiratory questionnaire In June 1993 the parents or guardians of the children completed a standard respiratory questionnaire, with questions on age, sex, ethnicity, country of birth, history of asthma or wheeze in the last 12 months, medication use, and also parents' occupations, history of asthma and smoking. The questionnaire included the question used in previous studies about the dietary consumption of fish - "How often does your child eat a meal that contains fish?" - with the options of replying "never or rarely", "once a week", or "more than once a week". Dietary questionnaire In October 1993, a food frequency questionnaire (adapted from that developed and validated by the Commonwealth Scientific and Industrial Research Organisation [CSIRO], Division of Human Nutrition, South Australia8,9) was distributed to the selected children, whose parents were asked to complete this for their child's usual eating habits over the last year. The questionnaire identified consumption patterns (daily, weekly, monthly, rarely or never) of more than two hundred foods commonly consumed in Australia. Additional questions on the type of fresh fish consumed and regular consumption of vitamin, mineral or herbal supplements were included. Estimates of sodium intake included naturally occurring sodium in foods, salt added in cooking, at the table and from processed foods. If questionnaires were not returned after one month the parents were contacted by telephone and offers were made to replace the questionnaires, or to provide assistance. In 11 cases, where neither parent spoke fluent English, an interpreter was commissioned to complete the questionnaire with the parents over the telephone. Returned dietary questionnaires were checked for missing or obviously erroneous information. Parents were contacted by telephone to complete omitted sections or to clarify erroneous information. Each food in the dietary questionnaire was allocated to one of 23 different food groups (see Appendix). Diets were analysed for energy, fibre and 39 nutrients (see Appendix). Definitions of respiratory categories, atopy, and categories of fish, plus a list of fish with more than 2% fat, are given in Box 1. Statistical analyses The questionnaires were analysed by the Division of Human Nutrition, CSIRO, South Australia, using Australian tables of nutrient composition12 for energy, protein, fat, carbohydrates, vitamins and minerals. The total quantity of food in each food group for every child was converted to a common base of weekly serves with Clinical Reporting Systems software.13 Data were analysed with the statistical package SAS.14The association between fish, food or nutrient intake and respiratory category was analysed categorically using chi-squared tests, and continuously using Student's t tests and analysis of variance. Some values obtained from the nutrient analysis were well outside what could reasonably be expected in children of this age group. These outliers were excluded from the statistical analysis. The number of exclusions never exceeded nine subjects in any analysis and were not significantly associated with any of the respiratory groups. Logistic regression was used to adjust estimates for the effects of known confounders for the effect of fish consumption on AHR and symptoms of asthma (e.g., sex, race, country of birth, atopy, early respiratory infection, parental smoking and parental asthma). Only those confounding factors found to be significant or approaching significance (P < 0.1) (atopy, parental asthma, early respiratory infection, country of birth) were included in the model. Results Of the 584 children selected 574 received the dietary questionnaire and 468 completed questionnaires were returned (81.5%). Non-responders were not significantly different from responders in the prevalence of AHR (26.0% v. 27.1%) or fish consumption (46.2% v. 52.1%). Box 2 shows details of the children studied. Children with current asthma did not differ significantly from children with normal airways in the consumption of any nutrient or food group. (Tables showing mean weekly intake in standard serves of food groups and mean daily intake [SD] of nutrients for children with normal airways and children with current asthma are available from the authors.) Children with wheeze only had a significantly higher intake of red meat (P < 0.05), offal meat (P < 0.001) and vitamin B12 (P < 0.03) and a significantly lower intake of mixed vegetables (P < 0.05) than children with normal airways. Children with AHR only consumed significantly more offal meat (P = 0.001) and high fat/high sugar foods (P < 0.001) than children with normal airways. They also had higher intakes of nitrogen, protein, total sugar, cholesterol, potassium nicotinamide, total nicotinamide, calcium, copper, zinc, vitamin B12 (P < 0.05) and refined sugar (P < 0.01). Total fish intake per week did not differ significantly between children with normal airways (1.2 serves per week; 95% confidence interval [CI], 1.0-1.3), AHR only (1.2 serves; CI, 0.9-1.5), wheeze only (1.2 serves; CI, 0.8-1.5) and current asthma (1.0 serve; CI, 0.8-1.2). Fresh fish was eaten by 84% (CI, 79.6%-88.4%) of children with normal airways, and by 72% (CI, 61.6%-82.4%) of children with current asthma. When fresh fish was divided into oily and non-oily types, significantly fewer children with current asthma (15.5%; CI, 7.1%-23.9%) included oily fish in their diet than did children with normal airways (30.8%; CI, 25.2%-36.4%; P < 0.05). There were no significant differences in the proportions of children with current asthma (56.3%; CI, 44.8%-67.8%) and normal children (52.9%; CI, 46.9%-58.9%) who ate exclusively non-oily fish. Neither fresh fish consumption nor respiratory disease was significantly associated with socioeconomic status, as defined by the father's occupation, or with the consumption of vitamin, mineral or other dietary supplements (including fish oil). The unadjusted risk (odds ratio) for children having current asthma was significantly lower in those who consumed any fresh fish or oily fresh fish (Box 3). Current asthma was found in only 8.8% (CI, 3.8%-13.8%) of children who ate oily fish, but in 15.6% (CI, 11.2%-20.0%) of those who ate non-oily fish only and 23% (CI, 14.2%-31.8%) of those who never ate fresh fish (Figure). When the results were adjusted for the effects of other known risk factors such as atopy, parental asthma, parental smoking, ethnicity, country of birth, early respiratory illness and sex, only children who ate oily fresh fish had a significantly reduced risk of current asthma. In these children, the risk was almost a quarter that of children who did not eat oily fish (odds ratio, 0.26; CI, 0.09-0.72) (Box 3). Consumption of any fresh fish, whether or not it was separated into oily fresh fish and non-oily fresh fish, did not significantly reduce the risk of AHR only or wheeze only either before or after adjustment for other risk factors. Discussion Our study shows that regular consumption of fresh, oily fish is associated with a reduced risk of current asthma. This reduced risk remained significant after adjustment for other known risk factors for asthma, including sex, atopy, parental asthma, parental smoking, early respiratory infection, ethnicity and place of birth. The subjects were selected from a random cross-sectional sample of children which was stratified (on the basis of recent respiratory symptoms and AHR to exercise) to increase the proportion of cases in the study group. The response rate was high (81.5%) and non-responders were not different from responders with respect to AHR or fish consumption. Socioeconomic status was not a confounder for either respiratory illness or fish consumption. Current asthma was defined as recent wheeze plus AHR to exercise. We have shown previously that current asthma, defined as recent wheeze plus AHR to histamine, identifies a group with severe, ongoing respiratory impairment, while those with AHR only and wheeze only have a milder condition which differs only slightly from the normal group.15 The diets of children with current asthma differed from those of the normal group only in the consumption of fresh, oily fish. In our previous study, more than one serve of fish per week was associated with a reduced risk of asthma,6 but in that study it was not possible to distinguish the effects of oily and non-oily fish. In the study reported here we were unable to detect differences in total fish consumption, possibly because of the smaller sample size. There were no significant differences between respiratory groups in the consumption of non-oily fish, suggesting that parents had not selectively withheld fish from the diets of asthmatic children. It is unclear why consumption of canned and processed fish was not associated with reduced risk of asthma. Processing may alter the integrity or activity of the fatty acids in fish oils. Several foods and nutrients in the diets of children with AHR only and wheeze only differed significantly from those of the normal group. However, none of these factors differed between the asthmatic and normal groups, suggesting that they are unlikely to have an aetiological role. Intake of offal meats was higher in both the AHR-only and wheeze-only groups, but, as offal meats are eaten by very few children, this may be a type I error. Vitamin B12 intake was also higher in both the AHR-only and wheeze-only groups, but the mechanism by which this could affect respiratory symptoms or AHR is unclear. There were no significant differences between any of the respiratory groups in consumption of sodium, vitamin C, vitamin E, selenium or magnesium. These findings do not support previous evidence that these dietary factors are important in the aetiology of asthma.4,5,16 Reduced risk of current asthma was associated with the consumption of oily fish, but not with non-oily fish. Fish oil contains the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which have anti-inflammatory effects.17 Theoretically, EPA could either prevent the development of asthma or reduce its severity by altering two of the cardinal features of asthma, namely airway inflammation and AHR. Supplementation with EPA reduces production of leukotriene B4,18 a chemical mediator responsible for the recruitment of inflammatory cells, such as neutrophils, into the airways. It also reduces production of the cytokine tumour necrosis factor (TNF),19 which increases airway responsiveness.20 Fish oil supplements given over 6-10 weeks cause a substantial uptake of EPA in neutrophil membrane phospholipids.18,21 In asthmatics, this may reduce the allergen-induced late asthmatic response,22 but does not change severity of asthma.21,22 However, a recent study suggests that a longer period of supplementation may be required to reduce asthma severity.23 Data of recent fish consumption (during the last 12 months) were used in our study, but may also reflect lifetime dietary habits. In conclusion, we have shown that consumption of oily fish is associated with a reduced risk of asthma in childhood. Although further studies are required to confirm these benefits, public health interventions to increase the consumption of oily fish may reduce the morbidity and prevalence of asthma in children. Appendix The 23 food groups were: cereals; dairy products; eggs; red, white, preserved meat and offal; seafood, fried, steamed, canned fish and fish fingers; red, green, white, mixed and other vegetables; legumes; high and low vitamin C fruit and other fruit; high sugar or fat content; and other. The 39 nutrients were: nitrogen; protein; starch; refined, natural and total sugar; total carbohydrate; saturated, monounsaturated, polyunsaturated and total fat; cholesterol; carotene; retinol; vitamin A; thiamine; riboflavin; potassium nicotinic acid and total nicotinic acid; niacin; vitamins B6 and B12; pantothenic acid; biotin; free and total folate; vitamins C, D, E; calcium; copper; iron; magnesium; manganese; phosphorus; potassium; selenium; sodium; and zinc. Acknowledgements This study was supported by the Fisheries Research and Development Corporation, Australia. The authors thank Dr Katrine Baghurst for allowing us to use the dietary questionnaire, Sally Record and Kay Pender for their help with the nutritional analyses, Elena Belooussova for data organisation and Suzanne Gray for her assistance with collecting the questionnaires. We are grateful for the support of the New South Wales Department of School Education, the Catholic Education Office and the Principals and teachers of all the schools involved. We are especially grateful to the parents and the children who participated in the survey. (©MJA 1996; 164: 137-140) References Robertson CF, Bishop J, Sennhauser FH, Mallol J. International comparison of asthma prevalence in children: Australia, Switzerland, Chile. Pediatr Pulmonol 1993; 16: 219-226. Burney P, Chinn S, Rona RJ. Has the prevalence of asthma increased in children? Evidence from the national study of health and growth 1973-86. BMJ 1990; 300: 1306-1310. Seaton A, Godden DJ, Brown K. Increase in asthma: a more toxic environment or a more susceptible population? Thorax 1994; 49: 171-174. Britton J, Pavord I, Richards K, et al. Dietary magnesium, lung function, wheezing, and airway hyperreactivity in a random adult population sample. Lancet 1994; 344: 357-362. Burney PG, Neild JE, Twort CHC, et al. Effect of changing dietary sodium on the airway response to histamine. Thorax 1989; 44: 36-41. Peat JK, Salome CM, Woolcock AJ. Factors associated with bronchial hyperresponsiveness in Australian adults and children. Eur Respir J 1992; 5: 921-929. Haby MM, Peat JK, Mellis CM, et al. An exercise challenge for epidemiological studies of childhood asthma: validity and repeatability. Eur Respir J 1995; 8: 729-736. Baghurst KI, Record SJ. Intake and sources in selected Australian subpopulations of dietary constituents implicated in the etiology of chronic diseases. J Food Nutr 1983; 40: 1-15. Rohan TE, Record SJ, Cook MG. Repeatability of estimates of nutrient and energy intake: the quantitative food frequency approach. Nutr Res 1987; 7: 125-137. Analyses of NSW fish and shellfish. Sydney: Australian Government Analytical Laboratory, 1989. Sinclair A, Dunstan GA, Naughton JM, et al. The lipid content and fatty acid composition of commercial marine and freshwater fish and molluscs from temperate Australian waters. Aust J Nutr Diet 1992; 49: 77-83. English R, Lewis J. Composition of foods Australia. 1st ed. Vols 1-5. Canberra: AGPS, 1989-1990. Clinical Reporting Systems [computer program], version 3.0. Sydney: Clinical Reporting Systems Pty Ltd. 1992. SAS [computer program], version 5. Cary, NC: SAS Institute, 1984. Toelle BG, Peat JK, Salome CM, et al. Toward a definition of asthma for epidemiology. Am Rev Respir Dis 1992; 146: 633-637. Stone J, Hinks LJ, Beasley R, et al. Reduced selenium status of patients with asthma. Clin Sci 1989; 77: 495-500. Kremer JM, Jubiz W, Michalek A, et al. Fish-oil fatty acid supplementation in active rheumatoid arthritis. Ann Intern Med 1987; 106: 497-503. Lee TH, Hoover RL, Williams JD, et al. Effect of dietary enrichment with eicosapentaenoic and docosahexaenoic acids on in vitro neutrophil and monocyte leukotriene generation and neutrophil function. N Engl J Med 1985; 312: 1217-1224. Endres S, Ghorbani R, Kelley VE, et al. The effect of dietary supplementation with n-3 polyunsaturated fatty acids on the synthesis of interleukin-1 and tumor necrosis factor by mononuclear cells. N Engl J Med 1989; 320: 265-271. Thomas PS, Yates DH, Barnes PJ. Tumor necrosis factor-alpha increases airway responsiveness and sputum neutrophilia in normal human subjects. Am J Respir Crit Care Med 1995; 152: 76-80. Arm JP, Horton CE, Mencia-Huerta J-M, et al. Effect of dietary supplementation with fish oil lipids on mild asthma. Thorax 1988; 43: 84-92. Arm JP, Horton CE, Spur BW, et al. The effects of dietary supplementation with fish oil lipids on the airways response to inhaled allergen in bronchial asthma. Am Rev Respir Dis 1989; 139: 1395-1400. Dry J, Vincent D. Effects of fish oil diet on asthma: results of a 1-year double blind study. Int Arch Appl Immunol 1991; 95: 156-157. (Received 31 May, accepted 28 Nov 1995) Authors' details Institute of Respiratory Medicine, Royal Prince Alfred Hospital, Sydney, NSW. Linda Hodge, MSc(Med), GradDipNutr&Diet, Dietitian. Department of Medicine, University of Sydney, Sydney, NSW. Cheryl M Salome, BSc, Senior Research Officer. Jennifer K Peat, PhD, Senior Research Officer. Michelle M Haby, MSc, Research Assistant. Wei Xuan, MSc, MApplStat, Statistician. Ann J Woolcock, MD, FRACP, Professor in Respiratory Medicine. Reprints: Professor A J Woolcock, Institute of Respiratory Medicine, Royal Prince Alfred Hospital, Camperdown, NSW 2050. (©MJA 1996; 164: 137-140)

Linda Hodge · Cheryl M Salome · Jennifer K Peat · Michelle M Haby · Wei Xuan · Ann J Woolcock

Viewpoint

Environmental health 5 February 1996 Free

Caring for a vulnerable population

Viewpoint Caring for a vulnerable population Who will take responsibility for those getting a raw deal from the health care system? Helen P Beange MJA 1996; 164: 159-160 Introduction - References - Author's details - - More articles on General practice and primary care Introduction In Australia, there is a minority population of about 70 000 people. Their mortality rate is at least 10 times that of the general population. They attend doctors twice as often, are admitted to hospital at twice the average rate, and have many more operations. More than half take prescription drugs daily, a third are taking multiple drugs, and 5% take more than four drugs. As 30% of this group have epilepsy, the commonest medications are anticonvulsants. On physical examination, they have an average of five serious medical disorders, but, astonishingly, only half of these conditions have been detected or treated. Although people in this minority group attend general practitioners frequently, they rarely see specialists, despite the fact that most of their disorders need specialist care. Blindness affects 4.4% (20 times the usual rate in Australia) and deafness affects 25% (compared with the average 2%) of people in this group, yet there are no special services for those who are blind or deaf. Although 9% have a psychiatric disability (compared with 2% of the general population), there are no special psychiatric services for them. Dental disease is the most frequent problem, affecting 86% of this group, but there are few special dental services. With such a gross difference in health when compared with the general population, it would be very reasonable to ask whether there are any modifiable risk factors for these diseases. The answer is yes -- surveys show that, while people in the group smoke very little and drink less than the general population, this minority group is generally unfit, obese and often hypertensive. So at least with exercise and better nutrition, it is likely they could avoid developing some diseases. Exercise opportunities improve the quality of life for people with an intellectual disability. (Reproduced with permission of the Stockton Centre, Newcastle, NSW.) How can this apparently disgraceful situation exist? Is Australia a Third World country? Is this a neglected and persecuted ethnic minority? No, not at all -- but this minority group does have problems accessing health care when compared with their fellow citizens. They are poorer and nearly all are dependent on social security. They tend not to marry or have children, and live mainly in public housing. Educational levels are low and illiteracy is the rule rather than the exception. They do not drive cars and many do not have an occupation. They are less mobile; 10% either need assistance to walk or use a wheelchair. One of the greatest barriers to health care is that many cannot speak at all and only half can communicate in complete sentences. The non-ideal social conduct of some of the group is such that doctors are nervous about keeping them waiting and reluctant to expose them to their other patients for fear of losing customers. Another barrier is that members of this group usually have to negotiate health care through another person, which only works successfully if their agent is trained and empathic and does not underestimate their complaints. Unfortunately, Australia has few doctors specially trained to understand this minority group. Australian doctors, although a decent lot, are (as a group) a bit impatient, are seldom able to fathom the language or unique culture of this group, and may not even recognise the names of most of the rare conditions from which they suffer. These conditions include fragile X syndrome, Rett syndrome and Angelman's syndrome. Further, because many of these patients take at least twice as long in consultation as the average patient, the more minority patients a doctor sees, the less the doctor's income. By now, you will have realised that the minority population I am concerned about is composed of people with an intellectual disability, which is defined as an IQ below 70. The figures given above are from a population study of adults between the ages of 20 to 50 in the lower North Shore of Sydney.1 All intellectually disabled adults living in a population of about 200 000 were identified and a random sample of 202 adults was examined. The lower North Shore is regarded as an affluent area of Sydney with good health services; it is thus reasonable to assume that conditions elsewhere in Sydney (and Australia) were either similar or worse. Studies on mortality and morbidity in people with intellectual disabilities in other parts of the world show similar results to the Sydney study.2,3,4 How can we improve the medical care of people with intellectual disabilities? I believe it is simplistic to think we can solve the problem by changing medical undergraduate training alone. Doctors currently treat intellectually disabled patients fairly well, but they are mainly dealing with minor illnesses and injuries. Serious problems are rarely recognised because these patients are used to suffering and cannot articulate their symptoms, and thus seldom complain. The woman with a slowly developing breast tumour, the man with anaemia as a result of a bleeding peptic ulcer, the child with Down's syndrome who is going deaf, the disturbed person having fluphenazine injections who is developing parkinsonism all depend on someone else to take them to a doctor. Young disabled people living at home are in less danger because there is a greater chance that their parents will badger the health system until something is done to help the child. But when a grown child leaves home, who will arrange medical care? Most Australian adults can be responsible for their own health, but we can rarely expect this of people with an intellectual disability. In the heyday of mental institutions, the medical superintendent was responsible for the health of people with an intellectual disability. Now, there is a question mark over just who is responsible. Local general practitioners, group home managers, area health service managers, heads of the Departments of Health and Community Services, perhaps even the Ministers, all disclaim responsibility. After all, the person is intellectually disabled, not sick. People with disabilities need access to the health system (a system which is becoming exceedingly complex). Once within the system, they need interpreters and advocates, and more time and resources than the average patient. General practitioners should obtain additional remuneration for the extra time spent with each patient. The health system needs to follow guidelines for improving the medical care of people with intellectual disabilities (see Box). The medical care of people with an intellectual disability should be set up in the mainstream of hospital medicine, not in academic backwaters. We need additional information about special health risks among people with disabilities and management protocols for the commonest syndromes. Preventive health services and health promotion would save enough money to make other special services available, such as dental clinics, psychiatric and neurological services and eye clinics. In the meantime, we are neglecting the health of people with developmental disabilities and, as a result, they are dying earlier and spending more time with doctors and more time in hospital than is necessary. If we valued the health of people with disabilities their lives would be longer and happier. References Beange H, McElduff A, Baker W. Medical disorders in adults with intellectual disability: a population study. Am J Ment Retard 1995; 99(7): 595-604. Fryers T. Mortality and cause of death. In: The epidemiology of severe intellectual impairment. The dynamics of prevalence. London: Academic Press, 1984: 139-141. Asberg KH. The need for medical care among mentally retarded adults. A five year follow up and comparison with a general population of the same age. Br J Ment Subnormality 1989; 35: 50-57. Howells G. Are the medical needs of mentally handicapped adults being met? J R Coll Gen Pract 1986; 36: 449-453. This article is based on a paper presented at the conference of the Australian Society for the Study of Intellectual Disability (NSW), Sydney, 12 May 1995. Author's details Stockton Centre, Developmental Disability Service, Hunter Area Health Service, Newcastle, NSW. Helen P Beange, MPH, FAFPHM, Visiting Medical Officer. No reprints will be available. Correspondence: Dr H P Beange, 23 Alpha Road, Willoughby, NSW 2068. Guidelines for improving medical care of people with intellectual disabilities Each patient with an intellectual disability should receive comprehensive and continuous health care, with primary care shared between clinical nurse specialists and general practitioners. They should have access to medical specialists and receive adequate attention in hospital. Clinical nurse specialists should be attached to the local group homes that are replacing institutional care. (Group homes usually house four people and are staffed either part-time or full-time.) These nurses would be responsible for health maintenance, preventive health care, arranging vaccinations and checking drugs. They would also make appointments for patients with acute and chronic health problems and maintain the medical records. General practitioners should be encouraged to review their disabled patients' drugs every three months and perform annual physical examinations. Full medical and genetic histories should be made available to these doctors. Health promotion clinics for people with disabilities should be established at teaching hospitals to provide back-up for the general practitioners in the area. These clinics should have formal links with genetic, paediatric and psychiatric departments and provide access to specialists who have expertise and empathy with disabled people. Clinics should offer medical, dietary and exercise advice, and opportunities for exercise after fitness testing. Protocols for dealing with particular syndromes should be developed (e.g., regular hearing and thyroid function tests for people with Down's syndrome, and regular surveillance for hip dislocation and urinary tract infections in people with cerebral palsy). All residential staff should be trained in basic health care, first aid, pharmaceutical treatment and nutrition. Staff should know how to treat fits and choking episodes. Courses in developmental disability medicine for medical students and interested family practitioners should be provided, utilising the skills of doctors who have experience in the field. A medical specialty in developmental disability medicine should be developed, so that these specialists could act as generalists in the same way as geriatricians care for the elderly. Back to text

Helen P Beange

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Editorials 19 February 1996 Free

How can we reduce heroin 'overdose' deaths?

Wayne D Hall

Research 19 February 1996 Free

Heroin-related deaths in New South Wales, 1992: toxicological findings and circumstances

Deborah Zador · Sandra Sunjic · Shane Darke

Health care 19 February 1996 Free

Recent changes in Australian general practice

Michael D Bollen

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Vaccine-preventable childhood diseases in Australia

Gavin W Frost · Monica Johns

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Drug-resistant Streptococcus pneumoniae: the beginning of the end for many antibiotics?

Peter J Collignon · Jan M Bell · the AGAR

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