Volume 175 Issue 3

Abstract Objective: To examine the relationship between compensation claims for psychiatric injury after motor vehicle accidents and physical injuries sustained. Design: Audit of Compulsory Third Party (CTP) insurance claims. Subjects and setting: 559 consecutive CTP claims referred by NRMA Insurance Limited to its sole provider of CTP legal services during a three-month period in 1994 after the claimant had engaged legal representation. Main outcome measures: Claim for psychiatric injury (any psychiatric disorder excluding traumatic brain injury) supported by a medicolegal report from a psychiatrist, other medical practitioner or psychologist; pre-existing psychiatric disorders; Injury Severity Score; initial treatment setting; hospital stay; percentage of accidents involving loss of consciousness or a death. Results: 522 claims were eligible for the study; 19.5% (102/522) included a claim for psychiatric injury. A pre-existing depression or anxiety disorder was documented in 11 claims (2.1% of all claims and 3.9% of those claiming psychiatric injury). Only very severe injuries, particularly those involving loss of consciousness, were associated with an increased rate of claims for psychiatric injury. Conclusions: No association was found between claims for psychiatric injury and severity of physical injuries, except among those most severely injured. More than 25 000 people are injured in motor vehicle accidents in New South Wales each year.1 Data from the NSW Motor Accidents Authority from 1998 show that about 60% of people who made a claim after a motor vehicle accident obtained legal representation,2 and that the percentage of claims with a psychiatric component rose from 2.2% to 8% between 1990 and 1998.3 NSW Motor Accidents Authority data also show that minor physical injuries result in 54% of all claims, but 77% of claims for psychiatric injury.3Motor vehicle accidents are associated with post-traumatic stress disorder (PTSD), other anxiety disorders and depression,4,5 although most recent publications refer to PTSD rather than other syndromes.4-9 However, the true incidence of PTSD and other disorders after these accidents is unclear; most studies have sampling bias and other methodological problems.4 The extent to which motor vehicle accidents cause the observed psychiatric disorders is also uncertain. Factors associated with PTSD include those not directly related to the accident, such as past psychiatric history6-9 and involvement in litigation,6,7 and others that are difficult to assess objectively, such as victims' recollections of fear of death6-10 and self-reported loss of consciousness.6,7 The relationship between PTSD and severity of physical injuries has also been investigated,6-13 with one study finding a positive correlation.7 In this study, I examined the relationship between compensation claims for psychiatric injury after motor vehicle accidents and physical injuries sustained. Methods Sample The sample comprised 559 consecutive claims on Compulsory Third Party (CTP) insurance that were referred by NRMA Insurance Limited to its sole provider of CTP legal services in a three-month period in 1994 after the claimant had engaged legal representation. All claims arose from motor vehicle accidents that occurred in New South Wales between 1989 and 1994. In this period, 39.5% of NRMA CTP claimants had legal representation. Of the 559 claims, 37 were excluded from the study as files were missing (25), the claim was from bereaved relatives (10) or the claimant had died since the claim (2). A further 50 files had data missing on one or more of the following: injuries, demographic details, or setting of medical care. As these files did not to appear to include claims for psychiatric injuries, they were included in denominators for proportions with psychiatric injury but were excluded from further analysis. Data collection and analysis I collected de-identified data from the files on systematic forms. The dependent variable was a claim for psychiatric injury (defined as any psychiatric disorder, excluding traumatic brain injury) supported by a report from a psychiatrist, other medical practitioner or psychologist. I recorded the presence of one or more of these injuries or traumatic brain injury attributed to the accident by the claimant's experts, as well as any pre-existing psychiatric disorder noted by claimants' or defendants' experts. Independent variables recorded were age and sex, type of motor vehicle accident and whether fatal (ie, any person killed), Injury Severity Score (ISS)14(calculated from information in the injury summary document in each file), setting of initial medical care (most medically intensive setting in the week after the accident), length of hospital stay, loss of consciousness during or after the accident (self-reported or corroborated), and self-reported neck or back pain (irrespective of physical or radiological signs). Data were analysed using the computer program SPSS.15 Logistic regression was used to determine the influence of independent variables on the presence of a claim for psychiatric injury. Results Most claimants (380; 73%) were passengers or drivers, and the remainder were motorcyclists, cyclists or pedestrians (92; 18%). The status of another 50 (10%) was not known because of incomplete files. Mean age was 34 years (range, 2-82 years), and 49% were male. Claims for psychiatric injury Claims for psychiatric or traumatic brain injury are shown in Box 1. One hundred and two people (19.5%) claimed at least one psychiatric injury related to the accident, combined with traumatic brain injury in six cases (another 11 people claimed traumatic brain injury alone). Thirty-six people claimed more than one psychiatric injury. Pre-existing psychiatric disorders are also shown in Box 1. These were documented in 25 people (4.8%), and comprised a depressive or anxiety disorder in 11 (2.1% of all claimants, and 3.9% of those claiming psychiatric injury). The reports supporting the psychiatric injury claims came from psychiatrists (65), psychologists (28) and other medical practitioners (9); mean time between the accidents and report dates was over two years. Experts disagreed on many claims, with treating practitioners and claimants' experts using the diagnoses of PTSD and depression (15% of claimants) more often than defendants' experts (2.5% of claimants), as described elsewhere.16 Variables associated with psychiatric injury claims The group that claimed psychiatric or traumatic brain injury had significantly longer hospital stay and higher mean ISS and proportion of accidents involving loss of consciousness than the group who claimed neither type of injury (Box 2). The group that claimed psychiatric injury but not traumatic brain injury also had significantly more accidents involving loss of consciousness and fatal accidents compared with those who claimed neither type of injury. There were no significant differences between the groups in proportions with self-reported neck or back pain. For the 102 who claimed psychiatric injury, the most medically intensive treatment in the week after the accident was provided by a local medical officer (33), in an emergency department (35), as a general inpatient (25) or in an intensive care unit (9). Psychiatric injury claims and injury characteristics are shown in Box 3 by initial treatment setting. The percentage of people who claimed psychiatric injury was significantly higher in those treated initially in intensive care than in those treated elsewhere (χ2 = 6.74; df = 1; P = 0.009). The percentage who claimed for PTSD and traumatic brain injury was also higher in the intensive care group (PTSD: χ2 = 8.99; df = 1; P = 0.003; and traumatic brain injury: χ2 = 103; df = 1; P <0.001). Mean ISS, hospital stay and percentage who reported loss of consciousness were also greater in those treated in more medically intensive settings (inpatient and intensive care), supporting the use of initial treatment setting as an indicator of injury severity. However, claims for neck or back pain were lower in claimants who received inpatient or intensive care treatment (Box 3). The percentage of people who claimed for a psychiatric injury did not increase with increasing ISS over the first nine deciles (mean, 20%). However, the percentage was significantly higher (33%) in people in the tenth ISS decile (ie, the most severely injured 10%) compared with those in the lower nine deciles (χ2= 4.34; df = 1; P = 0.04). A logistic regression analysis was performed using variables found to be significantly related to claims for psychiatric or traumatic brain injury by previous analyses (Box 4). Loss of consciousness and a fatal accident were significant predictors of claims for psychiatric injury. Discussion A claim for psychiatric injury was made in 19.5% of the legally represented CTP claims in this study, which is higher than the 4.6% estimated by the NSW Motor Accidents Authority for all victims of motor vehicle accidents during the same period.3 This confirms the previously reported association between psychiatric injury and legal representation.6,7 PTSD and depression were reported more often in this sample than in a recent survey of the Australian population.17 Conversely, pre-existing psychiatric disorders were documented much less often than the estimated prevalence of all psychiatric conditions in Australia (4.7% v. 17.7%17). This suggests that medicolegal assessments may under-report pre-existing psychiatric disorders and may sometimes wrongly identify a motor vehicle accident as the cause of a depressive or anxiety disorder that was actually pre-existing. In contrast to findings of the NSW Motor Accidents Authority,3 my study found that minor injuries were no more likely to be associated with a psychiatric injury than more severe injuries. However, a third of psychiatric injury claims (33/102) were made by people with physical injuries that were not severe enough for them to attend an emergency department or be admitted to hospital at the time of the accident. The study did find a positive relationship between the severity of physical injuries and claims for psychiatric injury in people who were very seriously injured. The psychological trauma of being severely injured may cause PTSD.5,7 Severe physical injuries may also cause psychiatric symptoms because of disability, pain or financial loss.5 However, in my study, the higher rate of claims for psychiatric injury in severely injured claimants was associated with loss of consciousness and involvement in a fatal accident rather than with other measures of injury severity. Reported loss of consciousness may be difficult to distinguish from amnesia resulting from emotional stress,18 which may predispose to psychiatric injury.19 The use of insurance claimants as the sample in this study led to selection bias and may have influenced the psychiatric injuries diagnosed by experts. The incidence and prognosis of whiplash injury are influenced by the system of assessing eligibility for compensation,20 and psychiatric injury may be similarly affected. More severely injured claimants may under-report their psychiatric symptoms because they are more concerned about their physical injuries and because the grounds for compensation for physical injuries have been clearly established. Claimants who are not seriously injured but are hurt or upset and have received less initial medical care may report more psychiatric symptoms. The opinions of expert witnesses may, in turn, be influenced by their role in the adversarial legal system.16 Under the current NSW system, some claimants may exaggerate their disability or genuinely become disabled because "significant disability" is a requirement for compensation;21 claimants who have a psychiatric injury but are less disabled are not compensated. Reform of the rules on expert evidence designed to reduce bias22,23 and a move to more detailed assessment of the cause of psychiatric symptoms after motor vehicle accidents may reduce the pressure for the NSW government to further limit psychiatric injury claims. Acknowledgements I would like to acknowledge NRMA Insurance Limited and Mr Victor Kelly of Abbott Tout Solicitors, Sydney, NSW, for making claimants' files available; Dr Timothy Heath (Concord Repatriation and General Hospital, Sydney, NSW) for his help with data analysis; and Dr Olav Nielssen (Psychiatrist, Sydney, NSW) for his assistance with the manuscript. The study was not funded. References Motor Accidents Authority and Roads and Traffic Authority of New South Wales. Road safety statistics, 2000. Available at <http//www.maa.nsw.gov.au/proftest/statistics/injury/report05.htm> (last sighted Jul 2001). Motor Accidents Authority and Road Traffic Authority of New South Wales. Compulsory third party statistics, 1999. Available at <http//www.maa.nsw.gov. au/professionals/statistics/CTP_stats_98.htm> Suhood S. Claims involving psychological disturbance, September 2000. Sydney: Motor Accidents Authority and Road Traffic Authority of NSW, 2000. Blaszczynski A, Gordon K, Silove D, et al. Psychiatric morbidity following motor vehicle accidents: a review of methodological issues. Compr Psychiatry 1998; 39: 111-121. Mayou R. The psychiatry of road traffic accidents. In: Mitchell M, editor. The aftermath of road traffic accidents. London: Routledge Press, 1997: 33-48. Ehlers A, Mayou RA, Bryant B. Psychological predictors of chronic posttraumatic stress disorder after motor vehicle accidents. J Abnorm Psychol 1998; 107: 508-519. Blanchard EB, Hickling EJ, Taylor AE, et al. Who develops PTSD from motor vehicle accidents? Behav Res Ther 1996; 34: 1-10. Mayou R, Bryant B, Duthie R. Psychiatric consequences of road traffic accidents. BMJ 1993; 307: 647-651. Ursano RJ, Fullerton CS, Epstein RS, et al. Acute and chronic posttraumatic stress disorder in motor vehicle accident victims. Am J Psychiatry 1999; 156: 589-595. Green MM, McFarlane AC, Hunter CE, Griggs WM. Undiagnosed post-traumatic stress disorder following motor vehicle accidents. Med J Australia 1993; 159: 529-534. Feinstein A, Dolan R. Predictors of post traumatic stress disorder following physical trauma: an examination of the stressor criterion. Psychol Med 1991; 21: 85-91. Bryant RA, Harvey AG. Initial posttraumatic stress responses following motor vehicle accidents. J Trauma Stress 1996; 9: 223-234. Blanchard EB, Hickling EJ, Taylor AE, Loos W. Psychiatric morbidity associated with motor vehicle accidents. J Nerv Ment Dis 1995; 183: 495-503. Baker SP, O'Neill B, Haddon W, Long WB. The Injury Severity Score: a method for describing patients with multiple injuries and evaluating emergency care. J Trauma 1974; 14: 187-196. SPSS for Windows. Release 9.0.1. Chicago: SPSS Inc, 1999. Large M, Nielssen O. An audit of medico-legal reports prepared for claims of psychiatric injury following motor vehicle accidents. Aust N Z J Psychiatry. In press. Henderson S, Andrews G, Hall W. Australia's mental health: an overview of the general population survey. Aust N Z J Psychiatry 2000; 34: 197-205. Kopelman MD. Fear can interrupt the continuum of memory. J Neurol Neurosurg Psychiatry 2000; 69: 431-432. Mayou RA, Black J, Bryant B. Unconsciousness, amnesia and psychiatric symptoms following road traffic accident injury. Br J Psychiatry 2000; 177: 540-545. Cassidy JD, Carroll LJ, Cote P, et al. Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Engl J Med 2000; 342: 1179-1186. Motor Accidents Compensation Act (NSW) 1999. Friston M. New rules for expert witnesses: The last shots of the medico-legal hired gun. BMJ 1999; 318: 1365-1366. Federal Court of Australia. Practice direction: guidelines for expert witnesses. Canberra: Federal Court of Australia, 1998. Available at <http://www. fedcourt.gov.au/pracproc/practice_direct.html> last sighted Jul 2001. (Received 31 Jul 2000, accepted 3 May 2001) Authors' details Department of Psychiatry, Royal Prince Alfred Hospital, Sydney, NSW. Matthew M Large, FRANZCP, Staff Specialist Psychiatrist. Reprints will not be available from the author. Correspondence: Dr M M Large, Department of Psychiatry, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050. mlargeATozemail.com.au Make a comment 1: Number of people claiming psychiatric or traumatic brain injuries and pre-existing psychiatric disorders among 522 insurance claimants Injury or disorder Injury claim Pre-existing disorder Traumatic brain injury (TBI) 17 (3.3%) 0 Post-traumatic stress disorder 48 (9.2%) 0 Depressive disorders 46 (8.8%) 8 (1.5%) Anxiety disorders 15 (2.9%) 3 (0.6%) Somatoform disorders 8 (1.5%) 3 (0.6%) Adjustment disorders 12 (2.3%) 0 Substance abuse 3 (0.6%) 4 (0.8%) Dementia or low IQ 0 3 (0.6%) Schizophrenia 0 2 (0.4%) Other 6 (1.1%) 2 (0.4%) Total* Psychiatric injury 102 (19.5%) 25 (4.7%) Psychiatric injury or TBI 113 (21.6%) 25 (4.7%) *36 people claimed more than one psychiatric injury. Back to text 2: Demographic, injury and accident characteristics among 472 insurance claimants* (95% CI) Variable No psychiatric or traumatic brain injury (n=359) Psychiatric injury (n=102) Psychiatric or traumatic brain injury (n=113) Age in years (95% CI) 33.4 (31.8-35.1) 36.4 (35.5-39.1) 35.7 (33.0-38.3) % Male 49% (44%-54%) 46% (36%-56%) 49% (39%-58%) Hospital stay in days 4 (3-5) 8 (4-12) 11 (6-16) Injury Severity Score† 11.7 (11.0-12.5) 14.0 (12.1-15.9) 16.1 (13.1-18.4) % With loss of consciousness 9% (6%-12%) 25% (16%-33%) 31% (23%-39%) % In fatal accident 1% (0-3%) 8% (3%-13%) 7% (2%-12%) % With neck or back pain 62% (57%-67%) 68% (59%-77%) 64% (55%-73%) Values in bold are significantly different from values for group with no psychiatric injury or TBI, as defined by non-overlapping 95% CIs. * 50 claimants were excluded from this analysis as no information was available on one or more of the following: nature of physical injuries, demographic details, or setting of medical care. † Maximum possible score, 75. Back to text 3: Psychiatric injury claims and injury characteristics among 472 insurance claimants,* according to initial treatment setting† (95% CI) Local medical officer (n=177) Emergency department (n=146) General inpatient (n=129) Intensive care unit (n=20) % With psychiatric injury 19% (13%-24%) 24% (17%-31%) 19% (12%-26%) 45% (26%-63%) % With post-traumatic stress disorder 10% (6%-14%) 10% (5%-15%) 8% (3%-12%) 30% (10%-50%) % With traumatic brain injury 0.6% (0-1.7%) 0.7% (0-2.0%) 5% (1%-8%) 45% (23%-67%) Mean Injury Severity Score 8.0 (7.5-8.5) 10.3 (9.5-11.0) 18.5 (17.0-20.0) 36.7 (31.3-42.0) Mean hospital stay (days) 0 1 13 (9-17) 40 (24-56) % With loss of consciousness 2% (0-4%) 12% (6%-18%) 27% (19%-35%) 60% (38%-82%) % With neck or back pain 81% (75%-87%) 71% (64%-78%) 33% (24%-41%) 20% (2%-38%) PTSD=Post-traumatic stress disorder. TBI=Traumatic brain injury. * 50 claimants were excluded from this analysis as no information was available on one or more of the following: nature of physical injuries, demographic details, or setting of medical care. † Most medically intensive treatment setting in the week after the accident. Back to text 4: Multivariate logistic regression analysis of variables potentially associated with psychiatric injury claims Odds ratio (95% CI) P Injury severity score* 0.98 (0.95-1.02) 0.29 ICU treatment 1.86 (0.80-4.35) 0.15 Hospital stay (days)* 1.00 (0.98-1.02) 0.45 Loss of consciousness 1.82 (1.20-2.88) 0.006 Fatal accident 3.47 (1.52-7.92) 0.003 ICU=Treatment in intensive care unit during first week. *Continuous variables. Back to text

Matthew M Large

MJA 2001; 175: 141-145 Abstract - Definitions - Prevalence - Severity - Lung function - GP consultation - Hospitalisation - Management - Morbidity and quality of life - Mortality - Discussion - References - Authors' details Make a comment - - - More articles on Psychiatry Abstract In 1997, 27% of Australian children had current wheeze, and this is increasing by 1.4% per year. The prevalence of wheeze among adults is lower and appears to be stable. The prevalence of persistent asthma (wheezing episodes with abnormal airway function between episodes) in children has increased from 5% to 9% in the past 20 years. In adults, the prevalence is 5%-6%. Up to 80% of adults with persistent asthma have abnormal lung function. Asthma deaths in Australia have fallen 28% since peaking in 1989, but the mortality rate is still twice that of England. The Australian Health Ministers' Conference in 1999 acknowledged the importance of asthma as a health issue by making it a National Health Priority Area. In the same year, the Cooperative Research Centre for Asthma (CRCA) was established. The CRCA is a joint venture between two medical research institutes (the Institute of Respiratory Medicine and the Garvan Institute of Medical Research), three universities (the University of Sydney, Monash University, and the University of Western Australia), six pharmaceutical companies, and the New South Wales Department of Health. Its mission is to reduce the burden of asthma on the Australian community. The three research programs of the CRCA are prevention of asthma, treatment of asthma, and diagnostic, delivery and monitoring devices. Here we summarise information on the burden of asthma in Australia and make some international comparisons. We do not attempt to develop a single estimate for the "burden" of asthma, but describe data on prevalence, severity, lung function, general practitioner and hospital attendances, management, morbidity, and mortality as related to asthma. Data on the prevalence of atopy are not presented. Although this is the strongest risk factor for asthma,1 its contribution to the burden of asthma is indirect. Definitions There is no agreed definition of asthma. The terms we use here are defined in Box 1. Asthma prevalence can be measured in terms of self-reported wheeze, doctor-diagnosed asthma, or a combination of symptoms and lung function abnormality.2 Moreover, asthma can be classified as intermittent or persistent, and persistent asthma can be classified into mild, moderate and severe, based on symptoms and degree of airway hyperresponsiveness.3 There are limitations to the use of questionnaires in the measurement of asthma. These arise because of differences between patients, parents, and doctors in the use of the label "asthma" and, to a lesser extent, "wheeze". Furthermore, substantial problems with recall bias may influence the findings. In evaluating questionnaire-based reports of the prevalence of asthma, it is important to be aware of the questions used to define asthma in the particular study. It is also relevant to be aware of assessments of the reliability and validity of the questionnaire. Prevalence Wheeze Children: Over the past 20 years, there have been at least 26 population-based studies measuring self-reported current wheeze in Australian children (Box 2). The prevalence of current wheeze has been increasing at a rate of 1.4% per year.4 The International Study of Asthma and Allergies in Childhood (ISAAC),19 in 38 countries across all continents, found that among children aged 6-7 years Australia had the second-highest prevalence of self-reported current wheeze (24.6%). Approximately a quarter of Australian children have wheezed in the past 12 months, and it seems unlikely that they all have intermittent or persistent asthma that requires treatment or is a burden. At present, there is no way to classify asthma on wheeze alone, although, in many studies, children with more than four wheeze episodes per year are regarded as having "asthma". Robertson et al4 found that among 6-7-year-olds who report current wheeze 34.7% reported more than four wheeze episodes (about 8% to 9% of the population). In comparison with other countries, Australia has the second-highest percentage of children aged 6-7 years who report more than four wheeze episodes in the previous 12 months.19 It can be calculated from the data reported by Bauman et al5 that children who wheeze are symptomatic about 14% of the time. Adults: In contrast to the information available for childhood wheeze, there is a paucity of data on the prevalence of current wheeze in Australian adults. Box 3 shows the prevalence of current wheeze to be between 17% and 29% in adults, with no apparent increase over time. In the European Community Respiratory Health Survey (ECRHS), conducted in 22 predominantly European countries, Australia had the fourth-highest prevalence of self-reported current wheeze in populations aged 20 to 44 years.20 Wheeze and lung function Objective measures of lung function combined with asthma symptoms allow classification of asthma into intermittent and persistent. Persistent asthma is clinically important asthma in that it causes more interference with work and school, requires more treatment, and results in more healthcare utilisation; hence, it represents a greater burden than intermittent asthma.2,27 In Australia, about 9%-11% of children6 and 5%-6% of adults21,22 have persistent asthma. Persistent asthma was not measured in phase one of the ISAAC study. The Australian reporting centre for the ECRHS found that 25.5% of its sample of adults in Melbourne had persistent asthma.28 However, the sample used in that study to determine prevalence of airway hyper-responsiveness (and thus persistent asthma) was not random, but was enriched with an additional 27% of symptomatic subjects. Although data on the prevalence of airway hyperresponsiveness have been published for the ECRHS as a whole, no data on the prevalence of symptoms together with airway hyperresponsiveness (ie, persistent asthma) have been published from this survey. Severity The measurement of severity of asthma is difficult. The nature of mild, moderate, or severe asthma depends on the perspective of the observer. Questionnaire assessments of severity generally focus on symptoms that are regarded by clinicians as indicative of more severe asthma, such as frequent wheeze episodes, severe episodes, hospital and emergency department admissions, and disturbed sleep. In addition, questions relating to disability and handicap arising from the disease, such as time off work or school and inability to carry out normal activities, are used as indicators of severity. None of these could be considered a "gold" standard. In the Australian data from the ISAAC study, among children aged 6-7 years with current wheeze 55.1% have nocturnal waking and 15.3% report severe wheeze episodes.4 In the international comparison, Australia ranked 10th highest for the percentage of children aged 6-7 years who had disturbed sleep in the previous year.19 Rosier et al29 used a statistical approach (item response theory) to develop a questionnaire-based functional assessment of disease severity in children with wheeze. In a population study, they found that the 14% of children who had current wheeze included 47% low, 18% mild, 30% moderate, and 5% high severity. This scale was validated by demonstrating correlations with school absence, functional impairment, practitioner consultations, and medication requirements. In the clinical setting, measurements of airway hyper-responsiveness are often used to determine asthma severity. Peat et al6 showed that of the Australian children with persistent asthma the percentage of children with severe airway hyperresponsiveness was less than 1%. Thus, it appears from both questionnaires and lung function data that the proportion of children with severe asthma is about 0.4%-0.6% of the population. The proportion of the burden of asthma that comes from the small group with severe asthma and from the larger group with mild asthma is open to interpretation. Health planners should target those with severe asthma, as they have a greater potential for adverse health outcomes30 and poorer long term lung function than individuals with intermittent asthma, many of whom remit.30,31 Lung function A proportion of the burden of asthma comes from symptoms of poor lung function. In their study of Busselton adults, Peat et al32 found that individuals with asthma have a more rapid decline of lung function over time compared with normal subjects. In that study, 86% of females and 82% of males with current asthma had abnormal lung function. A study of children in a suburb of an industrial city and in a rural town in New South Wales found that those who had airway hyperresponsiveness had reduced measurements of forced expiratory volume in one second (FEV1) over time.33 The magnitude of the burden of asthma due to poor lung function has not been documented. GP Consultation Data from the Bettering the Evaluation and Care of Health Study, 1998-1999,34 indicate that asthma is the sixth most frequently managed problem by GPs in Australia. Asthma is one of the top 20 reasons for individuals to visit a GP, with a rate of 1.4 per 100 encounters. Hospitalisation During the period 1998-1999, there were 53 907 hospital separations and 7464 same-day separations for asthma in Australia, equating to 147 496 patient-days.35 The average length of stay was 2.7 days. Faniran et al found that about 1.8% of children were admitted to hospital for asthma and 6.8% attended the emergency department in the previous year.7 In Australia, the ISAAC study found that for 6-7-year-olds who reported current wheeze about 7% were admitted to hospital and 14.4% attended the emergency department.4 Between 1998 and 1999, South Australia reported the highest hospitalisation rate (384 per 100 000 people) and Tasmania reported the lowest rate (148 per 100 000 people).35,36 Compared with countries with a similar high prevalence of wheeze, Australia has a very low rate of hospital admissions.37 The ECRHS study found that Australia had the third-lowest hospitalisation rate in adults with current doctor-diagnosed asthma. Only 1% of adults with asthma were admitted to hospital in the previous year. This might indicate that, comparatively, asthma in Australia is reasonably well managed, although many studies suggest that management is still not ideal.38,39 Management Correct prescribing practices and adherence to therapy are core issues in the management of asthma and quality of life, and thus the burden of asthma. One Australian study found that the use of anti-inflammatory medication was unsatisfactory in 26% of children with asthma.38 These children were treated either too aggressively or inadequately. Box 4 shows the patterns of treatment for children in Australia who reported wheeze episodes in the previous year.4 The degree of interventions increased in proportion to the number of wheeze episodes. However, for children who reported more than 12 wheeze episodes, both the use of inhaled steroids and the use of a written asthma action plan were inadequate. Perceptions of treatment efficacy and management among young adults (20-44 years old) in Victoria were examined in the ECRHS study.39 There was generally poor adherence to therapy among this age group. Adults in New Zealand and the UK also have a high prevalence of wheeze, but are three times more likely than Australian adults to take anti-inflammatory medication daily.37 It is difficult to ascertain how much of the GP and hospital attendances are indicative of poorly controlled asthma. Ruffin et al have shown that there is insufficient ownership of asthma management plans in South Australia.40 In 1996, only 33% of patients with asthma had an asthma action plan. Those who had action plans were more aware of asthma severity, used preventer medication more regularly, measured their lung function and understood their asthma. It is acknowledged that self-management plans result in improved health outcomes for patients with asthma.8 Furthermore, regular review and having a written asthma action plan contribute to reduction in hospital and emergency department attendances, and to reduced absenteeism from work or school and reduced nocturnal asthma.41 Morbidity and quality of life The Living with Asthma Study, conducted in 1999, found that asthma had a substantial impact upon child and adult lifestyles. Both groups felt tired and frustrated because of their asthma. One in five children did not ride a bike or play at school or with animals, and one in three did not participate in organised sport. One in four adults avoided socialising in restaurants, pubs and clubs because of the smoky environment. Parents of children with asthma were more anxious than parents of children who did not have asthma. The 1995 National Health Survey, conducted in a sample of the adult Australian population by the Australian Bureau of Statistics, included administration of the SF-36 (Short Form, 36 questions) questionnaire,42 which measures physical functioning, role limitations due to physical problems, bodily pain, general health, vitality, social functioning, role limitations due to emotional problems, and mental health. For all these categories, adults with asthma had lower mean scores than adults without asthma. The NSW Health Survey 1997 (Box 5) showed that many adults who have current doctor-diagnosed asthma suffer considerable morbidity.42 Mortality In 1998, there were 685 deaths from asthma in Australia (Box 6).44 This represents a 28% fall in asthma deaths since they peaked in 1989. The declining trend has occurred across all age and sex groups. Improved asthma management, implemented through the National Asthma Campaign, best explains this trend. There has been greater physician and patient testing of lung function and overall use of management plans. Despite improving mortality rates in Australia, the rate of 0.61 per 100 000 people aged 5-34 years is almost double that of England (0.35 per 100 000),45 indicating that there is still scope for improvement in asthma management practices. Discussion It is widely acknowledged that there are many sources of inaccuracy in studies of asthma prevalence.46,47 Even allowing for the various asthma definitions used in questionnaires, the data indicate that there is a large burden of asthma in Australia, in both children and adults. Moreover, for many measures of asthma, Australia has a high, if not the highest, prevalence when compared with other countries. However, large gaps remain in knowledge about the prevalence, severity and morbidity of persistent asthma in Australia and internationally. More information is needed about treatment practices and the groups of people most at risk for poor outcome. To accurately assess the burden, it will be necessary to relate asthma prevalence and severity to the indicators of morbidity and make international comparisons. There are many things that can be done now to reduce the burden of asthma. Patients and families can manage their own asthma by increasing their knowledge and awareness of asthma medication and control and removing barriers to adherence to treatment regimens. Clinicians should find efficient ways to diagnose and treat people with asthma, and form partnerships with patients to implement asthma management and action plans. Researchers should decide on useful definitions of asthma so that prevalence, severity and health outcomes can be compared with time and with changes in treatment practice. Although there is no cure for asthma, the disease can be controlled by good management. Improving quality of life and keeping prevalence, mortality and hospital admission rates low is well within the scope of clinicians and patients. This represents the preventable burden of asthma. Many questions about the burden of asthma, and how best to reduce it, remain to be answered. These include: What responsibility for reducing the burden of asthma should be borne by government, the National Asthma Campaign and asthma clinicians? How much of the burden is due to poor management by the doctor or individuals with asthma? Can asthma be prevented if treated early? Are there protective factors that can be introduced to reduce the prevalence of asthma? The Cooperative Research Centre for Asthma will address these questions and it is hoped that, together with other researchers, it will answer them. References Peat JK, van den Berg RH, Green WF, et al. Changing prevalence of asthma in Australian children. BMJ 1994; 308: 1591-1596. Toelle BG, Peat JK, Salome CM, et al. Towards a definition of asthma for epidemiology. Am Rev Respir Dis 1992; 146: 633-637. Global initiative for asthma. Global strategy for asthma management and prevention. NHLBI/WHO workshop report. March 1993. National Institutes of Health Publication No. 95-3659. National Heart, Lung and Blood Institute: Bethesda, Maryland, 1995. Available at <http://www.ginasthma.com/xwork.html> Robertson CF, Dalton MF, Peat JK, et al. Asthma and other atopic diseases in Australian children. Australian arm of the International Study of Asthma and Allergy in Childhood. Med J Aust 1998; 168: 434-438. Bauman A, Mitchell CA, Henry RL, et al. Asthma morbidity in Australia: an epidemiological study. Med J Aust 1992; 156: 827-831. Peat JK, Toelle B, Gray L, et al. Prevalence and severity of childhood asthma and allergic sensitisation in seven climatic regions of New South Wales. Med J Aust 1995; 163: 22-26. Faniran AO, Peat JK, Woolcock AJ. Prevalence of atopy, asthma symptoms and diagnosis, and the management of asthma: comparison of an affluent and a non-affluent country. Thorax 1999; 54: 606-610. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia, 1990 and 1993. Med J Aust 1996; 164: 403-406. Hurry VM, Peat JK, Woolcock AJ. Prevalence of respiratory symptoms, bronchial hyperresponsiveness and atopy in schoolchildren living in the Villawood area of Sydney. Aust N Z J Med 1988; 18: 745-752. Bauman A. Has the prevalence of asthma symptoms increased in Australian children? J Paediatr Child Health 1993; 29: 424-428. Henry RI, Abramson R, Adler JA, et al. Asthma in the vicinity of power stations: 1. A prevalence study. Pediatr Pulmonol 1991; 11: 127-133. Robertson CF, Heycock E, Bishop J, et al. Prevalence of asthma in Melbourne schoolchildren: changes over 26 years. BMJ 1991; 302: 1116-1118. Pearce N, Weiland S, Keil U, et al. Self-reported prevalence of asthma symptoms in children in Australia, England, Germany and New Zealand: an international comparison using the ISAAC protocol. Eur Respir J 1993; 6: 1455-1461. Gray EJ, Peat JK, Mellis CM, et al. Asthma severity and morbidity in a population sample of Sydney schoolchildren: Part 1 — prevalence and effect of air pollutants in coastal regions. Aust N Z J Med 1994; 24: 168-175. Robertson CF, Bishop J, Dalton M, et al. Prevalence of asthma in regional Victorian schoolchildren. Med J Aust 1992; 156: 831-833. Crockett AJ, Cranston JM, Alpers JH. The changing prevalence of asthma-like respiratory symptoms in South Australian rural school children. J Paediatr Child Health 1995; 31: 213-217. Volkmer RE, Ruffin RE, Wigg NR, Davies N. The prevalence of respiratory symptoms in South Australian preschool children. I. Geographic Location. J Paediatr Child Health 1995; 31: 112-115. Downs SH, Marks GB, Sporik R, et al. Continued increase in the prevalence of asthma and atopy. Arch Dis Child 2001; 84: 20-23. Worldwide variations in the prevalence of asthma symptoms: the International Study of Asthma and Allergies in Childhood (ISAAC). Eur Respir J 1998; 12: 315-335. Variations in the prevalence of respiratory symptoms, self-reported asthma attacks, and use of asthma medication in the European Community Respiratory Health Survey (ECRHS). Eur Respir J 1996; 9: 687-695. Peat JK, Gray EJ, Mellis CM, et al. Differences in airway responsiveness between children and adults living in the same environment: an epidemiological study in two regions of Australia. Eur Respir J 1994; 7: 1805-1813. Peat JK, Haby M, Spijker J, et al. Prevalence of asthma in adults in Busselton, Western Australia. BMJ 1992; 305: 1326-1329. Abramson M, Kutin J, Bowes G. The prevalence of asthma in Victorian adults. Aust N Z J Med 1992; 22: 358-363. Woods R, Wharton C, Walters H, Abramson M. The rising prevalence of asthma in young Victorian adults. Respirology 2000; 5 Suppl June: A26. Woods RK, Burton DL, Wharton C, et al. Asthma is more prevalent in rural New South Wales than metropolitan Victoria, Australia. Respirology 2000; 5: 257-263. Gibson PG, Mitchell C, Bauman A, et al. Asthma morbidity and management among adults in Australia, 1998. Respirology 2000; 5 Suppl June: A27. Van Asperen PP. Towards a better understanding of childhood asthma. J Paediatr Child Health 1995; 31: 272-275. Abramson M, Kutin JJ, Raven J, et al. Risk factors for asthma among young adults in Melbourne, Australia. Respirology 1996; 1: 291-297. Rosier MJ, Bishop J, Nolan T, et al. Measurement of functional severity of asthma in children. Am J Respir Crit Care Med 1994; 149: 1434-1441. Lange P. Prognosis of adult asthma. Monaldi Arch Chest Dis 1999; 54: 350-352. Martinez FD, Helms PJ. Types of asthma and wheezing. Eur Respir J 1998; 27: 3s-8s. Peat JK, Woolcock AJ, Cullen K. Rate of decline of lung function in subjects with asthma. Eur J Respir Dis 1987; 70: 171-179. Xuan W, Peat JK, Toelle BG, et al. Lung function growth and its relation to airway hyperresponsiveness and recent wheeze. Results from a longitudinal population study. Am J Respir Crit Care Med 2000; 161: 1820-1824. Britt H, Sayer GP, Miller GC, et al. Bettering the evaluation and care of health: general practice in Australia, 1998-99. Sydney: University of Sydney and Australian Institute of Health and Welfare, 1999. Australian Institute of Health and Welfare. Australian hospital statistics 1998-99. Canberra: AIHW, 2000. (AIHW cat. no. HSE 11. Health Services Series no. 15.) Australian Bureau of Statistics. Australian demographic statistics, March quarter 1999. Canberra: ABS, 1999. (Catalogue no. 3101.0.) Janson C, Chinn S, Jarvis D, Burney P. Physician-diagnosed asthma and drug utilization in the European Community Respiratory Health Survey. Eur Respir J 1997; 10: 1795-1802. Paterson NAM, Peat JK, Mellis CM, et al. Accuracy of asthma treatment in schoolchildren in NSW, Australia. Eur Respir J 1997; 10: 658-664. Reid D, Abramson M, Raven J, Walters EH. Management and treatment perceptions among young adults with asthma in Melbourne: The Australian experience from the European Community Respiratory Health Survey. Respirology 2000; 5: 281-287. Ruffin RE, Wilson D, Southcott A, et al. A South Australian population survey of the ownership of asthma action plans. Med J Aust 1999; 171: 348-351. Gibson PG, Coughlan J, Wilson AJ, et al. Self-management education and regular practitioner review for adults with asthma. The Cochrane Library. 2000(2): CD00117. Australian Bureau of Statistics. National health survey: SF-36 population norms. Australia. Canberra: ABS, 1995. (Catalogue no. 4399.0.) NSW Health Survey 1997 Electronic Report. <http://www.health.nsw.gov.au/ public-health/hs97/> Accessed 8 August 2000. Australian Bureau of Statistics. Causes of death: Australia. Canberra: ABS, 1998. (Catalogue no. 3303.0.) Twentieth Century Mortality. (England & Wales 1901 -1995) CD-ROM. London: Office for National Statistics, 1997. Kemp T, Pearce N, Crane J, Beasley R. Problems of measuring asthma prevalence. Respirology 1996; 3: 183-188. Magnus P, Jaakkola JJK. Secular trends in the occurrence of asthma among children and young adults: critical appraisal of repeated cross sectional surveys. BMJ 1997; 314: 1795-1799. (Received 11 Dec 2000, accepted 24 Apr 2001) Autors' details Cooperative Research Centre for Asthma, Royal Prince Alfred Hospital, Sydney, NSW. Ann J Woolcock, AO, FRACP, FAA, Principal Scientist (deceased); Shalini A Bastiampillai, Research Assistant; Guy B Marks, FRACP, FAFPHM, Project Leader. Victoria A Keena, BS Lib Sc, Information Manager. Reprints will not be available from the authors. Correspondence: Ms V A Keena, Institute of Respiratory Medicine, PO Box M77, Missenden Road, NSW 2050. vakATmail.med.usyd.edu.au Make a comment 1: Definitions Current wheeze A positive answer to the question "Have you [has your child] wheezed in the last 12 months?". Persistent asthma (sometimes called current asthma) Wheeze in the past 12 months together with evidence of abnormal airway function between attacks of wheezing. This abnormal function may include abnormal spirometry, abnormal waking peak flow values or airway hyperresponsiveness. Intermittent asthma Episodes of wheeze in the past 12 months with normal airway function between episodes. Burden of disease Burden can best be defined as the aggregate data from prevalence, lung function, practitioner consultations, hospital admission rates, poor management, quality-of-life indicators, mortality, and estimates of health-sector costs. Airway hyperresponsiveness An increased response to a provoking stimulus (usually inhaled methacholine or histamine), as measured by a 20% fall in forced expiratory volume in one second. Back to text Data are from reference 1, 4-18. The trend is calculated by averaging the prevalences for each year. Back to text Data are from references 8, 20-26. Back to text Back to text Back to text Back to text

Ann J Woolcock · Shalini A Bastiampillai · Guy B Marks · Victoria A Keena

Viewpoint Importance of retaining a national dietary guideline for sugar The Australian Dietary Guidelines are currently being revised and updated. There has been public discussion about the advisability of retaining a guideline for sugar because of insufficient evidence linking sugar consumption to ill health. However, there are concerns about the quality of the self-reported food intake data on which this conclusion is based. In addition, the doubling in diabetes prevalence in Australia in the past 20 years, which is linked to increased obesity from consumption of energy-dense foods, including those with added sugars (sugar-sweetened drinks being particularly important), provides a strong rationale for retaining a dietary guideline for sugar. Kerin O'Dea and J I Mann MJA 2001; 175: 165-166 A Working Group convened by the National Health and Medical Research Council's Health Advisory Committee is currently reviewing the Australian Dietary Guidelines, and reconsideration of the New Zealand dietary guidelines is also likely. Because of insufficient scientific evidence to link sugar consumption with ill health, a case has been made to abandon the guideline referring to sugar, "Eat only a moderate amount of sugar".1 Discussion of this issue is timely as sucrose consumption appears to be increasing. For example, New Zealand national nutrition surveys suggest that, between 1988 and 1997, self-reported sucrose intake increased on average from 42 to 62 g/person per day in males and from 27 to 45 g/person per day in females.2 Even more striking increases were evident in the age group 15-24 years. Dietary studies: Much of the evidence relating diet and disease comes from epidemiological studies, both cross-sectional and prospective. The nutritional and epidemiological methods currently available are insufficiently robust to accurately assess intakes and disentangle the effects of interrelated nutrients. Prospective studies have advantages over cross-sectional surveys, but there are still problems with assessment of dietary intake (which is usually only assessed on one occasion and by methods which are seriously flawed). Much of the evidence on which diet-disease relationships is based is self-reported, and there is substantial under-reporting of foods perceived to be unhealthy (eg, those rich in sugar, fat and alcohol). In particular, people who are obese tend to under-report, and do so selectively.3 Even randomised controlled clinical trials can be difficult to interpret, an excellent example being the CARMEN study.4 In this multicentre trial, 398 moderately obese adults were allocated at random to a seasonal control group (no intervention), a control diet group (dietary intervention typical of the average national intake), or one of two low-fat, high-carbohydrate groups (in which the carbohydrate was derived primarily from "simple" or "complex" carbohydrate). The weight changes on the latter two diets were not significantly different statistically, and the authors therefore concluded that the nature of carbohydrate is a relatively unimportant determinant of body weight. However, closer examination of the data reveals interesting trends: body weight loss on the low fat/high simple carbohydrate diet was 0.9 kg (P < 0.05) and on the high complex carbohydrate diet 1.8 kg (P < 0.001). A similar trend was apparent for change in fat mass. With a larger sample size, these differences might have become significant. Obesity and diabetes: The prevalence of obesity has risen sharply in Australia and New Zealand over the past 20 years. The recently released Diabesity and associated disorders in Australia 20005 draws attention to some of the devastating consequences of overweight and obesity. The association between type 2 diabetes and adiposity is arguably of even greater importance than the previously well described association with cardiovascular risk factors (hypertension and dyslipidaemia). Diabetes prevalence in the Australian adult population has doubled since 1980, the increase occurring in parallel with the rising prevalence of obesity. The estimated number of Australians with diabetes has reached almost one million, of whom less than 500 000 are aware of the diagnosis. The greatly increased risk of coronary heart disease and other vascular diseases, as well as the microvascular complications of diabetes (eg, retinopathy and nephropathy), emphasise the consequences of this disease, which has now reached epidemic proportions. This serious public health issue brings obesity to centre stage. It is caused by a complex interaction between genetic predisposition and environmental trigger factors, but the current epidemic of obesity has to be attributed to the "obesogenic environment"6 — the human genome has not changed in this period! The environmental facilitators of obesity are food intake and energy expenditure. While acknowledging the undoubted contribution of our increasingly sedentary lifestyle to the obesity epidemic, our discussion will focus on diet. Diet: Much of the discourse on the role of diet in the development of obesity highlights the role of fat, due to its high energy density (kJ/g of food or beverage) and its propensity, if consumed in excess, to be deposited as adipose tissue. However, there is now evidence that fat gain is similar with overfeeding of carbohydrate or fat.7 Energy intake is strongly influenced by energy density. Covert manipulation of energy density (ie, providing diets of different energy density without participants' knowledge) results in sustained changes in energy intake.8 The increased use of low-fat products, many of which are energy dense due to their high sugar content, and sugar-containing beverages now contributes significantly to total energy intake and are examples of the means by which sugar may enhance the energy density of the diet. If sugar does contribute to excessive energy consumption and to the problems of overweight and obesity, then clearly retention of a guideline is important. Evidence is accumulating that the form in which the sucrose is consumed is also important. A recent prospective study from Ludwig and colleagues9 showed a clear-cut, graded relation between the consumption of sugar-sweetened drinks and the development of obesity in children. The prevalence of obesity among children in the United States doubled between 1980 and 1994; 11% are now above the 95th reference percentile of body mass index (BMI) for age and sex. The observation that this increase paralleled the increase in sugar-sweetened soft drinks prompted Ludwig et al to enrol 548 ethnically diverse schoolchildren in four Massachusetts communities in a prospective study for 19 months. The difference in measures of obesity was related to change in consumption of sugar-sweetened drinks and other possible determinants of obesity, including physical inactivity and fat intake. For each additional serving of sugar-sweetened drinks both BMI (mean, 0.24 kg/m2) and frequency of obesity (odds ratio, 1.6) increased, after adjustment for anthropometric, demographic, dietary and lifestyle variables. Changes in diet soft drink intake were not related to obesity incidence. Of course, an observational study does not prove causality, but it is of interest that another recently published study in an entirely different group of older individuals produced similar results. Elmslie and coworkers10 compared a group of bipolar (manic depressive) patients and matched controls; the patient group had higher rates of overweight and obesity than the controls. The bipolar patients reported a higher energy intake, the increased energy being derived almost entirely from sucrose in sweetened drinks. Energy from drinks (regardless of whether it is from sugar, fat or alcohol) adds to total energy intake, and does not displace energy from other forms.11 Furthermore, compensation at subsequent meals for energy consumed in the form of liquid (drinks) appears to be less complete than for energy consumed in solid form (food) (ie, people overconsume more easily when excess energy is in the form of energy-containing beverages).12 While these new data suggest an obesity-promoting effect of sugar-containing beverages, it may also be relevant to recall data published some 30 years ago.13 Middle-aged men were asked to replace, as far as possible, sucrose with foods rich in starch to maintain energy balance. Despite regular advice and encouragement from a dietitian they were unable to maintain energy balance and lost weight, presumably because of the greater satiety-promoting qualities of the starchy foods. While not providing direct evidence for sugar as an aetiological factor, these observations do suggest that recommending a reduction in sugar may be a potentially useful public health measure in countries where obesity and its comorbidities have reached epidemic proportions. Implications for Indigenous populations: Our discussion has particular significance for Australian and New Zealand Indigenous populations, who have very high rates of lifestyle-related chronic diseases occurring at much younger ages than the non-Indigenous population.14,15 Indigenous people often have poor-quality diets, high in sugar and fat, and depleted in fruit and vegetables. For example, Lee and coworkers16 analysed the food supply at six remote Aboriginal communities in the Northern Territory using the "store turnover" method, and found a very high consumption of sugar per se and in soft drinks. The diets had high levels of animal fat (mainly from poor-quality meat) and very low levels of fruit and vegetables (ie, energy-dense and nutrient-poor). Most of the sucrose was consumed in liquid form as sugar in tea and in carbonated beverages. Retention of a dietary guideline for sugar: The evidence we have assembled here leads us to strongly advocate the retention of a dietary guideline for sugar in Australia and New Zealand. In fact, given the marked rise in consumption of carbonated beverages in Australia over the past 30 years (47.3-114.4 L/person per year between 1968-69 and 1996-97), we also advocate an addition: "Consume only moderate amounts of sugars and foods and beverages containing added sugar". This is in line with the recently revised US dietary guidelines,17 which include the recommendation "Choose beverages and foods that limit your intake of sugars". There is also a strong population health rationale for mandatory labelling of foods with clear information, including sugar, fat, and total energy content. References Williams P. Sugar: is there a need for a dietary guideline in Australia? Aust J Nutr Diet 2001; 58: 26-31. New Zealand food: New Zealand people. Key results of the 1997 National Nutrition Survey. LINZ Activity and Health Unit, University of Otago for the Ministry of Health. Dunedin, NZ: University of Otago, 1999. Heitmann BL, Lissner L. Dietary underreporting by obese individuals - is it specific or non-specific? BMJ 1995; 311: 986-989. Saris WHM, Astrup A, Prentice AM, et al. Randomized controlled trial of changes in dietary carbohydrate/fat ratio and simple vs complex carbohydrates on body weight and blood lipids: the CARMEN study. Int J Obesity 2000; 24: 1310-1318. Dunstan D, Zimmet P, Welborn T, et al, on behalf of the AusDiab Steering Group. Diabesity and associated disorders in Australia: the accelerating epidemic. Report of the Australian Diabetes, Obesity and Lifestyle Study. Melbourne: International Diabetes Institute, 2001. Egger G, Swinburn B. An "ecological" approach to the obesity pandemic. BMJ 1997; 315: 477-480. McDevitt RM, Poppitt SD, Murgatroyd PR, Prentice AM. Macronutrient disposal during controlled overfeeding with glucose, fructose, sucrose or fat in lean and obese women. Am J Clin Nutr 2000; 72: 369-377. Stubbs RJ, Johnstone AM, O'Reilly LM, et al. The effect of covertly manipulating the energy density of mixed diets on ad libitum food intake in "pseudo free-living" humans. Int J Obesity 1998; 22: 980-987. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective observational analysis. Lancet 2001; 357: 505-508. Elsmlie J, Mann JI, Silverstone JT, et al. Determinants of overweight and obesity in patients with bipolar disorder. J Clin Psychiatry 2001; 62. In press. Poppitt SD, Prentice AM. Energy density and its role in the control of food intake: evidence from metabolic and community studies. Appetite 1996; 26: 153-174. Mattes RD. Dietary compensation by humans for supplemental energy provided as ethanol or carbohydrates in fluids. Physiol Behav 1996; 59: 179-187. Mann JI, Truswell AS, Hendricks D, Manning EB. Effects on serum lipids in normal men of reducing dietary sucrose or starch for five months. Lancet 1970; 1: 870-872. Daniel M, Rowley KG, McDermott R, et al. Diabetes incidence in an Australian Aboriginal population: eight year follow up study. Diabetes Care 1999; 22: 1993-1998. Simmons D, Harry T, Gatland B. Prevalence of known diabetes in different ethnic groups in inner urban South Auckland. N Z Med J 1999; 112: 316-319. Lee AJ, O'Dea K, Mathews JD. Apparent dietary intake in remote Aboriginal communities. Aust J Public Health 1994; 18: 190-197. Nutrition and your health: dietary guidelines for Americans. 5th edition, 2000. Home and Garden Bulletin No 232. Washington, DC: Department of Agriculture, Department of Health and Human Services; 2000. Authors' details Menzies School of Health Research, Darwin, NT. Kerin O'Dea, PhD, Professor and Director. University of Otago, Dunedin, New Zealand. J I Mann, PhD, DM, FRACP, Professor in Human Nutrition and Medicine. Reprints will not be available from the authors. Correspondence: Professor Kerin O'Dea, Menzies School of Health Research, PO Box 41096, Casuarina, NT 0811. kerinATmenzies.edu.au Make a comment

Kerin O'Dea · J I Mann