Volume 180 Issue 10

Announcing the Dr Ross Ingram Memorial Essay Competition (entry details below) Not so long ago, we at The Medical Journal of Australia realised that, when it came to Indigenous health, we were great at publicising the problems. Most of the articles we publish are observational studies confirming that, yes, in health, as well as in almost every other area, Indigenous Australians are worse off than other Australians and, indeed, Indigenous populations worldwide. Ross Ingram (16 Feb 1967 – 15 May 2003) Ross Ingram was an Indigenous doctor who died last year, aged 36, of cardiovascular disease. At the time of his sudden death he was working as a GP in the New South Wales rural town of Leeton. Ross grew up in the Leeton area, where he was educated at the local primary and high schools. In 1984 he was named Young Citizen of the Year for Leeton, and in 1985, while vice-captain of Leeton High School, he received a Rotary Citizenship Award. In 1987 he was awarded a National Aboriginal Islander Day Observance Committee (NAIDOC) Award for Aboriginal Youth of the Year. Ross was the first Indigenous person from NSW to be accepted into the University of Newcastle’s Medical School. He enrolled in 1986 and graduated in 1993, the first Wiradjuri person to become a doctor. Life and medicine took him to an internship and residency in Gosford, then general practice on the NSW central coast and in Tasmania, and finally back to practise in Wiradjuri Country (central western New South Wales). His death is the first among the small community of Indigenous doctors who have been graduating from Australian medical schools since 1984. A keen practitioner of softball, football and cricket, as well as medicine, Ross was proud of his achievements both as a man and an Indigenous man. He is remembered by a loving family, including his wife, Julie, three children and three stepchildren. We also realised that the Journal was missing an important “voice”, telling us the story of Indigenous health. Many of the people working in Indigenous healthcare do not publish in academic journals. Also, more than in some other sectors of the population, social, cultural, political and economic issues influence the health and wholeness of Indigenous people. Some of these factors cannot be explored in strict academic style. Essays, on the other hand, leave room for the writer to analyse and interpret, often from a personal perspective and possibly including some form of narrative — “telling a story”. With this in mind, we are delighted to announce the annual Dr Ross Ingram Memorial Essay Competition for the best essay relating to Indigenous health. The competition is open to any Indigenous person who is working, researching or training in a health-related field; we are looking for essays that present original and positive ideas aimed at promoting health gains and health equity for Australia’s Indigenous peoples. After all, real insights and solutions come from within, not from without. The essays should be no more than 2000 words long, and must be submitted by Monday, 10 January 2005. A panel, including external experts and MJA editorial staff, will judge finalist essays, and judges will be blinded to the identities of the authors. The judges’ decision will be final. The winning entry will be published in the 2005 Indigenous Health issue of the Journal (the second issue in May), and the author will receive $5000. Other essays of high merit may also be published. We asked the members of the Australian Indigenous Doctors’ Association (AIDA) to help us name the prize and they chose to name it after Dr Ross Ingram (see Box). Ross’s story of premature death from natural causes is not an unusual one. More than half the deaths in Indigenous men occur before they reach the age of 50, compared with 13% of deaths among non-Indigenous men. The members of AIDA chose Ross not just because he was the first known Indigenous doctor to die, but because his plight typified that of many of the people currently working in Indigenous health. The human reality of statistics like those mentioned above is that Indigenous Australians inhabit a world of sickness, death and tragedy. Many of the seeds of future ill health are present from before birth. To a greater extent than most of their non-Indigenous colleagues, Indigenous doctors risk becoming a part of the problem they are trying to treat. “As Indigenous doctors, the fraternity of medicine has always accepted us wholly, and without question, and yet we are very different from so many of our non-Indigenous colleagues. Many doctors, when they look into the eyes of an Indigenous child, get a glimpse of a world they never knew existed; when we look into the eyes of that child, we see ourselves, and are reminded of the toll taken by unending stress and anxiety, and cycles of grief. For Indigenous doctors, the loss of our dear brother Ross reminds us that the privilege we enjoy as doctors does not remove our responsibilities to our people.” — Louis Peachey, President, AIDA We are hoping that the Dr Ross Ingram Memorial Essay Competition will provide a forum for some of the stories and ideas of Indigenous people working in Indigenous healthcare. Ross Ingram will not be able to contribute in this way, but he is a silent reminder of both the problem and the struggle of those who are working to find a solution. We look forward to receiving your entries.

Ruth M Armstrong BMed · Martin B Van Der Weyden MD, FRACP, FRCPA

Consensus is yet to be reached on the optimal approach to screening Australians have a 1 in 21 lifetime risk of developing colorectal cancer.1 The incidence of the disease and mortality resulting from it can be reduced by population-based screening programs, as has been demonstrated in several large randomised controlled trials of faecal occult blood testing (FOBT).2 The Bowel Cancer Screening Pilot Program currently under way in Queensland, South Australia and Victoria is assessing the practical application of FOBT. While screening of asymptomatic, average-risk individuals for colorectal cancer is advocated by many authorities worldwide (including the National Health and Medical Research Council [NHMRC] in Australia1), uncertainty remains as to the screening test of choice. The numerous publications on the subject are indeed like jigsaw pieces waiting to be put together to reveal the complete picture. In addition to FOBT, the NHMRC-recommended screening options for asymptomatic, average-risk individuals include flexible sigmoidoscopy (FS), and it is timely to review its role here. Colonoscopic studies on asymptomatic people show that 60% of adenomas and cancers occur in the distal colon and are potentially detectable by sigmoidoscopy. Case–control studies have shown that sigmoidoscopy can reduce the risk of subsequent fatal distal colorectal cancer by up to 60%, translating to an approximate 30% reduction in overall colon cancer mortality.3 Direct evidence of the magnitude of benefit from randomised controlled trials that are currently under way is awaited. A 5-yearly screening interval is recommended, based on data from these ongoing studies (which suggest that benefit from sigmoidoscopy extends up to 10 years) and on studies of repeat colonoscopy (which show that significant neoplasia is very uncommon 5 years after polypectomy or a normal examination). What are the performance characteristics of FS? The procedure is typically done in an unsedated patient after administration of an enema and takes 5–10 minutes to perform. At our institution, generally eight procedures are done by one operator over 2 hours. The instrument is advanced as far as is tolerated with reasonable comfort (mean insertion depth, 60 cm; range, 30–110 cm4) with biopsy or removal of polyps performed at the time. The finding of any adenomatous polyp or other suspicious lesion prompts further evaluation with colonoscopy. Fifteen percent of such screenings result in referral for colonoscopy.5 However, some have suggested that diminutive adenomas may not require follow-up — a policy that might reduce colonoscopy referrals to 5% of screenings.6 FS is a safe procedure, with a reported colonic perforation rate of about 1 in 50 000.7 Outpatient colonoscopy, which includes therapeutic procedures, has a perforation rate of about 1 in 1000.8 Concerns are commonly raised about the potential miss rate of FS for lesions in the proximal colon beyond the reach of the instrument and of small lesions that are overlooked in the areas examined. Many heterogeneous studies have addressed the issues of missed proximal colonic lesions and of what distal colonic findings should trigger colonoscopic follow-up. The likelihood of a proximal advanced polyp (ie, one with pathological features that increase malignant potential, such as size or villous architecture) increases with a more advanced distal finding. In the absence of any distal adenoma, 2%–5% of asymptomatic people screened will have isolated proximal advanced lesions.9 Whether this is acceptable in the context of cancer screening may become clear from prospective studies. The fact that sigmoidoscopy may also miss lesions within the area of colon that is examined may have implications for the screening intervals used. It has been shown on repeat FS that polyps may be missed in up to 20% of cases,10 while with colonoscopy a 6% miss rate for adenomas larger than 1 cm has been reported.11 Schoen et al12 recently reported a 0.8% advanced adenoma or cancer rate (there were 6 cancers in 9317 repeat examinations) in patients having a repeat examination 3 years after an apparently normal examination; 80% of advanced lesions were in regions thought to have been adequately examined previously, indicating missed or newly evolved lesions. However, other studies have shown that after 5 years the rate of new findings is low enough to consider lengthening the screening interval.5 The technical aspects of FS are sufficiently clear to enable us to define what FS can and cannot do. From the point of view of screening, FS clearly cannot completely exclude the presence of colon cancer in all asymptomatic people. A distinction must be made between screening the general population and testing the individual seeking screening. For the former, obtaining the greatest mortality benefit safely and at an acceptable cost to the nation is the crux of the matter. Recently published data indicate that FS is a cost-effective screening strategy, although colonoscopy and annual FOBT avert a greater number of cancer deaths.13 The results of randomised controlled trials of screening FS and colonoscopy, currently being conducted, will allow us to make a more accurate comparison with the established data regarding FOBT. Participation rates in sigmoidoscopy screening (23% in initial screening and 54% in follow-up screening at our institution) are encouraging given the invasive nature of FS screening.4,5 The ability of Australian gastroenterologists to accommodate increased demand for colonoscopy, whether as a follow-up to FOBT or FS, remains to be seen. Pieces of the jigsaw continue to fall into place, although it is likely to be some years before a clearly superior screening modality is determined. The emergence of new technologies such as virtual colonoscopy14 and faecal genetic testing will continue to add to the available armamentarium.

Charlie H Viiala MB BS, FRACP · John K Olynyk MB BS, FRACP, MD

Although some vaccines new to the childhood schedule are not free, they are strongly recommended In September 2003, the National Health and Medical Research Council (NHMRC) approved the new Australian Standard Vaccination Schedule recommended by the Australian Technical Advisory Group on Immunisation (ATAGI) (Box). The schedule includes inactivated poliomyelitis vaccine (IPV), varicella vaccine and seven-valent pneumococcal conjugate vaccine (7vPCV) for infants and young children. Earlier, in late 2002, routine meningococcal C conjugate vaccine was approved and funded for children aged 12 months, together with a cross-sectional catch-up program for young people to the age of 19 years (media release, Senator Kay Patterson, 24 November 2002). For the first time since 1994 — when all vaccines recommended on the schedule were funded for children vaccinated by both private and public providers under the National Immunisation Strategy1 — the childhood schedule recommended by NHMRC contains vaccines (IPV, varicella and 7vPCV) not available free of charge to parents. As well as adding these four vaccines to the childhood program, the NHMRC also approved changes to the pertussis vaccination schedule. Since the diphtheria–tetanus vaccine was replaced by a combined diphtheria–tetanus–acellular pertussis (DTPa) vaccine at 4–5 years in 1995, the peak age of pertussis has progressively risen to 13–18 years.2 Based on recent evidence that three doses of DTPa in the first year of life provide good protection until the age of 6 years,3 it was decided to adjust the schedule so that the fifth dose is now given to adolescents at 15–17 years, using an adult-formulated vaccine (dTpa). This was done by removing the 18-month dose, thus making the 4-year dose the fourth dose. This is not expected to lower preschoolers’ protection from pertussis,4 but should help reduce the number of large local reactions seen when the dose was given at 18 months.5 Inactivated poliomyelitis vaccine was recommended because it does not cause the extremely rare (1 in 2.4 million doses) live-vaccine-associated paralytic polio. The United States has already changed to inactivated vaccine,6 and other countries are considering doing so. The change to this vaccine in Australia may take time, as it is many times more costly than the oral vaccine and has had limited availability. Although various combinations of IPV with diphtheria, tetanus, acellular pertussis, Haemophilus influenzae type b and hepatitis B vaccines are licensed in Australia,7 they are not yet available, as the companies producing them are uncertain of the potential market. In the interim, the Australian Government’s National Immunisation Program will continue to provide free oral live-attenuated poliomyelitis vaccine. In making recommendations about the inclusion of each new vaccine in the childhood vaccination schedule, ATAGI took into account a wide range of factors. These included: vaccine safety and efficacy; the preventable burden of the disease targeted by the vaccine; the ease with which the vaccine could be integrated into the existing schedule; any likely effects on herd immunity, reduction in antibiotic resistance or impact on disease epidemiology; and cost-effectiveness and equity issues. Some of the information used by ATAGI as the basis for its recommendations is contained in the The Australian immunisation handbook (8th edition), while the levels of evidence for the new recommendations are available on the Internet and on CD-ROM.7 NHMRC resolved that the benefits of these vaccines were sufficient for them to be included in the schedule, irrespective of the provision of public funding. These new vaccines are more costly than any previous additions to the vaccination schedule. In the private market, three doses of conjugated pneumococcal vaccine cost far more than $300, one dose of varicella vaccine more than $40 and combinations with IPV more than an extra $18 for the IPV component. At the government level, the total annual cost of adding IPV, varicella vaccine and 7vPCV to the schedule would be about $100 million, and would almost double the current cost of all other childhood vaccines. This is a large expenditure. The cost-effectiveness of these three vaccines in Australia is therefore important.8-10 Changing to IPV (at $14 per dose) is estimated to prevent one case of vaccine-associated paralytic polio every 2–3 years, a cost of $17 million per case averted.8 This must be considered in the context of the maintenance of public confidence in immunisation programs. For varicella vaccine (at $53 per dose), universal vaccination of infants could prevent 450 hospitalisations each year, at a cost of $21 000 per hospitalisation averted, and one death per year, at a cost of $10 million per death averted, over a 30-year period.9 This does not include the out-of-pocket costs to families of a child having varicella, which make vaccination cost-effective in the United States.11 Universal use of 7vPCV (at $90 per dose) could prevent two to three deaths, 13 cases of meningitis, 110 cases of invasive pneumococcal disease, 800 cases of pneumonia and 14 600 cases of otitis media which would otherwise occur annually in each birth cohort of about 240 000 non-Indigenous Australian children by their fifth birthday.10 The cost per death averted and the cost per life-year saved by 7vPCV is estimated to be $5 million and $230 000, respectively.10 This does not take into account the impact of universal 7vPCV on adult pneumococcal disease or pneumococcal antibiotic resistance, as documented in the United States.12 However, these economic data were only part of the many reasons that ATAGI and NHMRC recommended that all children receive these vaccines (see above). Parents should be strongly encouraged by their physicians to have their children vaccinated. Conjugated pneumococcal vaccine is funded for a small group of children with medical conditions placing them at high risk of disease, as well as for Aboriginal and Torres Strait Islander children.7 For some parents the NHMRC recommendation will be sufficient; for others further discussion of the vaccine costs and benefits will be needed. Detailed fact sheets to assist providers and parents are available on the website of the National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases <www.ncirs.usyd.edu.au>. Until all recommended vaccines are available free at the point of service, there is a dilemma for the community and for policy makers. The objectives of high childhood vaccine coverage and of equity for children could be at stake. This will be a continuing issue over the next 5–10 years as more new vaccines become available. These include rotavirus vaccine, live attenuated intranasal influenza vaccine, and other live vaccines targeting viral respiratory pathogens. Until now, vaccines have had a very high cost–benefit ratio, often being cost-saving,13 in contrast to many other prophylactic and most curative treatments. We can no longer expect vaccines to be cost-saving, with the increasing cost of the large clinical trials now needed to measure impact on rare diseases and to exclude rare adverse effects. Nevertheless, despite the fall in cost–benefit ratio in absolute terms, the economic benefits of vaccines relative to pharmaceuticals will persist.13 We now need greater public awareness of the current and potential benefits of disease prevention from vaccines, leading to greater public advocacy. Maximal benefit from vaccines can only be obtained by ensuring their availability and use across all age-eligible members of the population. Australian standard vaccination schedule7

Margaret A Burgess MD, FRACP, FAFPHM · Peter B McIntyre FRACP, FAFPHM, PhD

Objective: To quantify the burden of disease and injury for the Aboriginal and non-Aboriginal populations in the Northern Territory.Design and setting: Analysis of Northern Territory data for 1 January 1994 to 30 December 1998 from multiple sources.Main outcome measures: Disability-adjusted life-years (DALYs), by age, sex, cause and Aboriginality.Results: Cardiovascular disease was the leading contributor (14.9%) to the total burden of disease and injury in the NT, followed by mental disorders (14.5%) and malignant neoplasms (11.2%). There was also a substantial contribution from unintentional injury (10.4%) and intentional injury (4.9%). Overall, the NT Aboriginal population had a rate of burden of disease 2.5 times higher than the non-Aboriginal population; in the 35–54-year age group their DALY rate was 4.1 times higher. The leading causes of disease burden were cardiovascular disease for both Aboriginal men (19.1%) and women (15.7%) and mental disorders for both non-Aboriginal men (16.7%) and women (22.3%).Conclusions: A comprehensive assessment of fatal and non-fatal conditions is important in describing differentials in health status of the NT population. Our study provides comparative data to identify health priorities and facilitate a more equitable distribution of health funding.

Yuejen Zhao BMed, MBiostats, PhD · Steve Guthridge MB BS, MTH, FAFPHM · Anne Magnus BEc, BEd · Theo Vos MD, MSc

Objective: To examine long-term trends in cancer mortality in the Indigenous people of the Northern Territory (NT) of Australia.Design: Comparison of cancer mortality rates of the NT Indigenous population with those of the total Australian population for 1991–2000, and examination of time trends in cancer mortality rates in the NT Indigenous population, 1977–2000.Participants: NT Indigenous and total Australian populations, 1977–2000.Main outcome measures: Cancer mortality rate ratios and percentage change in annual mortality rates.Results: The NT Indigenous cancer mortality rate was higher than the total Australian rate for cancers of the liver, lungs, uterus, cervix and thyroid, and, in younger people only, for cancers of the oropharynx, oesophagus and pancreas. NT Indigenous mortality rates were lower than the total Australian rates for renal cancers and melanoma and, in older people only, for cancers of the prostate and bowel. Differences between Indigenous and total Australian cancer mortality rates were more pronounced among those aged under 64 years for most cancers. NT Indigenous cancer mortality rates increased over the 24-year period for cancers of the oropharynx, pancreas and lung, all of which are smoking-related cancers.Conclusions: Cancer is an important and increasing health problem for Indigenous Australians. Cancers that affect Indigenous Australians to a greater extent than other Australians are largely preventable (eg, through smoking cessation, Pap smear programs and hepatitis B vaccination).

John R Condon MPH, FAFPHM, PhD Student · Joan Cunningham ScD · Tony Barnes MSc · Bruce K Armstrong DPhil

Objectives: To determine the incidence rate of coronary heart disease (CHD) in Australian Aboriginal people with type 2 diabetes, and to compare the impact of diabetes on CHD risk in Aboriginal women and men.Design: Cohort study.Setting: A remote Aboriginal community in the Northern Territory.Participants: 889 Aboriginal people aged 20–74 years followed up to 31 May 2003 after baseline examination in 1992–1995.Main outcome measures: Incidence rates of CHD (estimated for 123 participants with diabetes at baseline and 701 “non-diabetes” participants); rate ratios for diabetes risk (95% CI), with “non-diabetes” participants as the reference group.Results: Participants with diabetes at baseline had a higher rate of CHD (37.5 per 1000 person-years) than those without diabetes (7.3 per 1000 person-years). Adjustment for multiple CHD risk factors, such as age, smoking, alcohol consumption, systolic blood pressure, body mass index, high-density lipoprotein cholesterol and total cholesterol levels, resulted in a CHD rate ratio for women of 3.7 (95% CI, 1.6–8.9) (comparing women with diabetes with those without) and a CHD rate ratio for men of 1.4 (95% CI, 0.4–4.1) (comparing men with diabetes with those without).Conclusions: Aboriginal women with diabetes experienced a significantly higher risk of CHD than women without diabetes. Although the difference was not statistically significant, women with diabetes had a higher CHD risk than men with diabetes.

Zhiqiang Wang PhD · Wendy E Hoy MB BS, BScMed, FRACP

Objective: To assess primary care processes and clinical characteristics of adults with diabetes in remote northern Australian Indigenous communities.Design: Clinical audit from diabetes registers in 21 remote primary healthcare centres in the Torres Strait Health Service District (n = 921), three in Cape York, Queensland (n = 252), and three in the Northern Territory (n = 194), between September 2002 and February 2003.Participants and setting: Aboriginal and Torres Strait Islander adults with diabetes who were receiving their routine diabetes care in these 27 centres.Main outcome measures: Provision of regular checks for weight, blood pressure, glycaemia (HbA1c), proteinuria, lipid levels, renal function, eyes and feet, influenza and pneumococcal vaccination. Weight, blood pressure and glycaemic control.Results: Most routine diabetes checks were delivered according to recommended schedules, except for eye and foot checks in the NT. There were uniformly high rates of appropriate treatment for hypertension and albuminuria, but low rates of insulin treatment and self-monitoring despite a high mean HbA1c level (8.9%). Vaccination rates were low in the NT. Torres Strait Islanders with diabetes were significantly heavier than Aboriginals, but had lower mean diastolic blood pressure (77.3 mmHg compared with 79.5 mmHg) and lower prevalence of albuminuria and smoking.Conclusion: A high proportion of Aboriginals and Torres Strait Islanders requiring treatment for high blood pressure and proteinuria are receiving it. However, there is dissonance between the relatively high rates of routine checks and apparent lack of therapeutic action on glycaemia. More intensive management of glycaemia, including improved nutrition, exercise and (probably) insulin, is required to reduce microvascular complications.

Robyn A McDermott FAFPHM, PhD · Fiona Tulip AssocDipMRA · Barbara Schmidt BSc, MBA

Fairness and compassion are the bases for improving Aboriginal health There is no dispute that Aboriginal health in Australia is both poor and very much worse than that of non-Aboriginal people, and their life expectancy at birth is about 21 years less for men and 19 years less for women. Among Aboriginal and Torres Strait Islander males, 6.8% die in infancy, compared with 1% for the rest of the population. For females the figures are 6.7% and 0.8%. A large array of diseases are much more prevalent among Aborigines.1 Institutional racism in Australian healthcare — some examples Funding inequity: Overall funding of Aboriginal healthcare is not commensurate with extra need.8 Different performance criteria for black and white: For example, in Perth, Derbarl Yerrigan Aboriginal Medical Service funding was cut when an “overspend” arose because of success in attracting clients; at the same time the teaching hospitals’ overspend was 120 times as great as that at Derbarl Yerrigan. The teaching hospitals were given an extra $100 million to cover their overspend.9 “Body part” funding: For instance, separate streams of money for conditions such as diabetes and heart disease for a health service which is intended to be holistic — 26 funding streams (and hence 26 separate accounts and 26 demands for accountability) for the Danila Dilba Aboriginal Medical Service in Darwin. Differences in treatment regimens: Aboriginal people in Western Australia born in the 1940s received low-cost nursing care; in contrast, a white cohort of the same age received higher-cost technological care.10 Inequitable Medicare Primary Health Care (Medicare Benefits Schedule plus Pharmaceutical Benefits Scheme): In Katjungka (a remote Aboriginal community), $80 per head per year; in Double Bay (an affluent Sydney suburb), $900 per head per year.11 Cultural barriers to Aboriginal use of healthcare services: Inadequate funding to reduce these barriers (such as language barrier and lack of recognition of different constructs of health) for Aboriginal people. This is not news. The question is how to improve this situation. The argument presented in this article rests on two core and related ideas: that our health services are “institutionally racist” and that such racism stems from Australia being, or at least having become, an uncaring society. The way forward that we propose is recognising and addressing institutional racism. This would provide a framework for improving Aboriginal health. We believe, however, that acceptance of the need to address such racism can only come about through building a more compassionate and decent society. To suggest that healthcare in Australia is institutionally racist may be confronting for some, but we argue not only that it is institutionally racist, but, more importantly, that such racism represents one of the greatest barriers to improving the health of Aboriginal and Torres Strait Islander people. We will also indicate what might be done to overcome this institutional racism and improve Aboriginal health. Defining institutional racismInstitutional racism “refers to the ways in which racist beliefs or values have been built into the operations of social institutions in such a way as to discriminate against, control and oppress various minority groups”.2 It has been claimed that “Institutional racism is embedded in Australian institutions”.3 Often, institutional racism is covert or even unrecognised by the agents involved in it. In recent years, interest in both the concept and practice of institutional racism has increased. In the United Kingdom, it was sparked by the Stephen Lawrence Inquiry,4 published in 1999. This examined the events which followed the completely unprovoked murder in 1993 of Stephen Lawrence, a young black man, which was “unequivocally motivated by racism”. It found that the investigation was marred by a combination of professional incompetence, institutional racism and a failure of leadership by senior officers. It claimed that “officers approached the murder of a black man less energetically than if the victim had been white and the murderers black”. In the context of racial and ethnic disparities, Camara Jones,5 an Assistant Professor at Harvard University School of Public Health, has called for “a growing national conversation on racism”, one key aspect of which is “institutionalized racism”. This she sees as being “often evident as inaction in the face of need”. An increasing focus on institutional racism in Aotearoa (New Zealand) was prompted by a visit there by Camara Jones in 1999.6 In Australia, institutional racism has been an almost constant feature of our history, from the British designation of the continent as terra nullius, through the 1897 Convention on Federation (where the question of whether Aboriginal people should be counted as “people” in the national census was covered in just 195 words7), to the stolen generations and the failure of the federal government to issue an apology. Examples of institutional racism are shown in the Box. Clash of culturesWe believe that any healthcare system is a social institution built on the cultural stance of the population it serves. It follows that cultural values should provide the value base for health services. Between Aboriginal and non-Aboriginal Australians, there is not only a difference in culture, but a clash of cultures. We think some white people are at least dimly aware of this. However, the extent of their understanding of the difference between a culture based on individualism, where the individual ranks above the community in importance, and a communitarian culture, in which each individual is less important than the whole, is limited. One of us, S H,7 a Gungulu man, has written: “Aboriginal Peoples have built a communitarian solidarity that includes an awareness and affirmation of the [cultural] difference [of Aboriginal people]. Such communitarian solidarity is a form of civic friendship between peoples that is distinguishable from other forms of friendship because it unites people who are members of the same particularistic cultural community — persons who share a common worldview and use the same primary moral vocabulary.” Yet that value base is inadequately recognised in the planning of healthcare services in this country. Where societies or social entities have a greater awareness of and concern for mutuality, reciprocity and sharing, trust in institutions will be fostered and racism will diminish. Many Australians have embraced the individualism of neoliberalism. Uniting as a community around little other than the successes of its sporting teams, today’s white Australia lacks these “communitarian” traits. While communitarianism need not always be a force for good (the Nazi vision of the “master race” is a case in point), it can be and has been a beneficial force in Aboriginal culture. Here it is best seen in terms of what the distinguished public servant Coombs12 describes as “the Aboriginal ethic of accountability to others”. This, he writes, “is required by their commitment that autonomy, at a personal and group level, will be exercised so as to ensure that what is done contributes to the care and nurture of others with whom they are related; so that personal behaviour remains socially grounded”. In current health policy there is little attempt to recognise the differences in culture between black and white. The holism of Aboriginal health involves not just a “wholeness”, but a series of mutual obligations. Aboriginal Medical Services attempt to provide culturally “secure” services (ie, services based on Aboriginal preferences where differences in culture do not create additional barriers to use). Their poor funding levels, however, severely restrict them in this. Mainstream services make almost no effort to understand or provide culturally secure services. To deliver such services might increase primary healthcare costs for Aboriginal people by more than 50%.9,13 This is because, for example, questioning with respect to history has to be indirect, and preceded by time spent in building trust and confidence between the doctor and patient. This process, to be done well, can be time consuming. Also, advocacy on behalf of the client with other agencies, such as those providing housing, is often expected by Aboriginal clients as part of a GP’s role. The prospects for creating a cohesive Australian community, advancing social capital, furthering equity and reducing racism are not bright. For example, the Human Rights and Equal Opportunities Commission conducted a series of consultations across Australia which showed racism to be widespread and institutionally based, especially with respect to Aboriginal people.14 We believe that the current Australian federal government puts at risk our social capital in its pursuit of divisive policies. This applies not only to Aboriginal people, but also to other minority groups, defined racially or otherwise. For example, extending upfront fees for universities gives the affluent greater access compared with the poor; and ignoring the principle of universality (which did not rate a mention in the Prime Minister’s media release as one of his three pillars of Medicare15) on Medicareplus creates yet more of a two-tier healthcare system. The government’s policies on immigration have been severely criticised by many, including Father Frank Brennan, the Jesuit priest and lawyer, who concludes his book on the subject with an appeal to re-create social capital in Australia: “Many of us would like to return collectively to being a warm-hearted, decent international citizen.”16 We believe that Aboriginal people have lost their trust in the institutions of government, including healthcare services. Lack of respect by white Australians for Aboriginal values, the discounting of these values by those who have sought, patronisingly and paternalistically, to “do good” to Aboriginal people (according to a “good” defined by white fellas), leads to further erosion of trust. The lack of trust by Aboriginal people in white people and white institutions is obvious. More tellingly, we believe there is a lack of trust by Aboriginal people in themselves as a people — a lack of confidence in their culture. It is this last, a legacy of colonisation and its aftermath, that has wreaked the greatest havoc of all. We also believe that there is a lack of political will and of leadership to deal with inequalities generally in Australian healthcare. The most glaring example in recent times lies in the government’s schemes to promote private health insurance. The cost of increasing spending on primary healthcare for Aboriginal people to a level which would take into account such considerations as greater health problems, cultural-access barriers and equity (ie, increasing it to five times the per-capita level for non-Aboriginal people17) might be measured by the benefit forgone if the government were to halve the rebate (from 30% to 15%) for private health insurance.18 Progressing from institutional racismCurrently, cultural differences and ignorance create racism, and indifference nurtures it. Cultural differences must be celebrated, rather than denigrated. Former Prime Minister Paul Keating’s Redfern Speech on reconciliation pointed the way forward: “I think what we need to do is open our hearts a bit. All of us. Perhaps when we recognise what we have in common we will see the things which must be done . . . If we open one door others will follow.”19 That was 12 years ago. Today, the converse is true. As we have closed one door, others have followed. So many doors on social justice are closing in this society. We closed the door on a Norwegian freighter carrying abandoned refugees. We close the door on children in detention centres, on poor youngsters trying to get a university place. We close the door on opportunities for Aboriginal people and on the richness of an ancient culture which is potentially there for all Australians to learn from and take pride in. What scope is there for building compassion? Not much, it might seem, in this neoliberal society and this globalising world. Yet, as the social commentator Richard Titmuss remarked 30 years ago about the UK National Health Service, altruism and compassionate acts are infectious not only to other people, but to other events and circumstances.20 Compassion is good for us. What to do?Firstly, white Australia must learn to understand Aboriginal culture, particularly with respect to its fundamental philosophy of “communitarian solidarity”. Only then can social institutions, such as healthcare services for Aboriginal people, be built on a genuine understanding followed by accommodation of the hopes and aspirations of Aboriginal people. More directly, only then can Aboriginal people have the chance to have health services delivered to them that are, by right, as accessible (in the broadest sense) as they are to white Australians. Secondly, those white people who were described (above) as patronising and paternalistic would cease to be so when, in their “doing good”, good was defined by Aboriginal preferences. Thirdly, Aboriginal communitarian preferences must drive Aboriginal health services, their funding and their performance indicators. Unless the governance of Aboriginal organisations is based on Aboriginal cultural values, these services will not function effectively or efficiently. Fourthly, public compassion must be built into the Australian social fabric. The “fair go”, if it ever existed, has gone, but Australia needs a leadership that will articulate that fair go. The philosopher Martha Nussbaum argues against “impoverished models of humanity” with “numbers and dots taking the place of women and men”.21 She continues: “. . . when one’s deliberation fails to endow human beings with their full and complex humanity, it becomes very much easier to contemplate doing terrible things towards them . . . if you really vividly experience a concrete human life, imagine what it is like to live that life, and at the same time permit yourself the full range of emotional responses to that concrete life, you will . . . be unable to do certain things to that person. Vividness leads to tenderness, imagination to compassion.”21 Finally, our call is for a more compassionate society. Attitudes to asylum seekers, to Aboriginal people, to people who are in any way disadvantaged, are linked. Social attitudes need to be more compassionate to all who are disadvantaged, and not just to Aboriginal people. ConclusionAboriginal people merit so much more from white Australia. First and foremost, they deserve white Australia’s trust — trust that Aboriginal people know better than white Australians what is good for Aboriginal people. They deserve (and not just in their music and dancing) recognition of their culture. Two things are necessary — first, Australian society needs to listen and hear the calls of the disadvantaged (and there are so many in Australia today, especially Aboriginal people); then, those who have compassionate voices need to use them. Many people working in healthcare and in universities have social consciences and believe in social justice. They need not only to give voice to the voiceless, but to give themselves voice as decent, white Australians. In this Australia — this divided, divisive, racist, socially unjust society that we have built — we now need institutions and policies that will unbuild it. We need to acknowledge that the “fair go” is struggling to survive, if not already dead. Fairness and compassion need to be once again the guiding principles of our leaders and our democracy. Only then can we build a society where decency can become the fundamental in addressing Aboriginal health. There will be no sudden breakthrough; there is no magic pill. Decency, however, is a good place to start.

Barbara R Henry GradDipHE · Shane Houston PhD · Gavin H Mooney MA

During the 1950s and 1960s, there was a dramatic explosion in the number of letters to the editor about Indigenous health published in the MJA, reflecting increased reader interest. The letters from Barry Christophers were part of the Federal Council for Aboriginal Advancement’s largely successful campaign for equal civil rights for Aboriginal and Torres Strait Islander people. His letters not only drew attention to discriminatory legislation and policies, but also emphasised the structural (especially economic) determinants of Indigenous ill-health, and the negative impact on Indigenous people of racist medical representations. There was little interest in the health of Aboriginal and Torres Strait Islander peoples in the MJA before 1950. Early research portrayed Aboriginal people as being from an inferior and primitive race, the demise of which was thought to be inevitable. For example, in 1924, a case series of Aboriginal psychiatric patients was introduced by stating that: Contact with civilization, phthisis and other diseases, mixed breeding and general racial decay are the order of the day. In a few years this line of research will be closed for ever. Whatever may be one’s sentimental views on the passing of the primitive peoples, from the scientific or even the utilitarian aspect it will be more than unfortunate if our records are not completed before they vanish.1 Any research on Aboriginal and Torres Strait Islander peoples before the 1960s was not primarily about improving their health. It was about using Indigenous health research to improve understanding of the health problems of white Australians, and about collecting information about Aboriginal people for science before the race became extinct.2 Letters to the editor are the voice of the readers of the MJA. Letters do not have the same academic status as journal articles, but three readership surveys in the 1950s and 1960s showed that the letters pages were the most read section of the MJA.3-5 An editorial marking the 50th anniversary of the MJA in 1964 described the number of letters to the editor as a barometer of the interest of readers in a journal.6 Most letters received by the MJA were published.7 Before 1950, there were only 13 letters about Indigenous Australians published in the MJA. Readers did not write more than a single letter to the editor in response to any MJA publication about Indigenous people until 1952, when an editorial announced that a new university scholarship for an Aboriginal student marked a change from the brutal past of the colonial encounter, and decried the obstacles caused by “the monstrous fiction of racial superiority and inferiority”.8 Writers of editorials had much greater freedom of language and freedom to express opinions than writers of scientific articles. Letter writers had even more freedom, and were often those with the strongest opinions. Four letters were published in response to the editorial: one claimed that it was possible to discuss Aboriginal people’s inferiority (but did not assert a biological basis for this inferiority); the others replied that doctors should treat “aborigines as our equals” and that their problems were due to racism.9-12 A dramatic increase in letters to the editor about Indigenous health began in the 1950s (Box 1). This increase occurred before a large increase in the number of all letters later in the decade. Letters to the editor accounted for a quarter (48/200) of the publications on Indigenous health in the MJA in the 1950s and 1960s, increasing to more than a third in the 1980s and 1990s (76/204 and 108/203).2 Barry Christophers’ letters to the MJA editorBarry Christophers (Box 2) wrote 25 letters to the MJA about Indigenous health between 1956 and 1969. He wrote half the letters to the editor about Indigenous health in this period (and a similar number of letters not about Indigenous health), but he did not write any longer articles about Indigenous health. At the time, Christophers was a general practitioner in the inner-city Melbourne suburb of Richmond, and an activist in the Federal Council for Aboriginal Advancement (FCAA) (in 1964 the name was changed to the Federal Council for the Advancement of Aborigines and Torres Strait Islanders [or FCAATSI]) (Box 3). His letters may not have reflected the views of the majority of MJA readers, but they draw attention to one doctor’s role in events that led to great changes in the relationship between Indigenous and non-Indigenous Australians. In 1957, Christophers drew MJA readers’ attention to claims of starvation in the Warburton Ranges made by Pastor (later Sir) Doug Nicholls and Western Australian members of parliament William Grayden and Stan Lapham.16,17 He often sent similar versions of his MJA letters to various newspapers, but he saw a special role for doctors. He explained to me that he wrote to the MJA because doctors were “important folk in the community” who influenced people’s views and attitudes (Dr Barry Christophers, personal communication). Christophers was always careful to not criticise the work of individual doctors; his targets were governments and bureaucrats, and their discriminatory policies and legislation. He did not choose to either alienate his audience or undermine the authority of the medical voice, which could continue to be used for other activities. In contrast, other writers in the MJA questioned the capacity of non-medically trained activists like Nicholls to speak authoritatively on Indigenous health matters.18 Christophers wrote many letters to the MJA about FCAA and FCAATSI campaigns to highlight and then remove discriminatory legislation and policies affecting Indigenous people. He wrote about the restriction of the movement of Aboriginal people in Western Australia by the “leper line”.19,20 He wrote four letters to the MJA, and many more to newspapers, supporters, bureaucrats and politicians, about the exclusion of Queensland Aboriginal patients with tuberculosis from the generous allowance paid to other TB patients to encourage convalescence and treatment.21 He explained that the exclusion was “understandable”, even if abhorrent, only because it was much higher than the very low wages then being paid to Aboriginal people in northern Australia.22 Christophers was secretary of FCAA’s Equal Wages Committee and, in the MJA and elsewhere, he repeatedly emphasised economic causes (and solutions) for Indigenous people’s suffering and ill-health. While many of his contemporaries blamed Aboriginal behaviour, just as their predecessors had blamed Aboriginal people’s inferior racial characteristics, Christophers focused on deeper structural causes of ill-health. In response to a claim that alcohol restriction needed to continue and citizenship to be opposed, he argued that Aboriginal alcohol abuse was merely a “symptom” of the “disease” of “lack of citizenship, low wages and colour prejudice”.23 In spite of his attention to structural determinants of health, he did not portray Indigenous people as passive victims; their actions were constrained, but not entirely determined, by racist, white institutions; nor did they just drift or follow biological urges, as others had claimed. His concern with the WA “leper line” was due to its interference with the attempts by Aboriginal “liberators” to “assist some of their not so fortunate friends”.20 Aboriginal people could be their own liberators and the liberators of other Aboriginal people, not just a problem to be solved by others. In the Northern Territory, he complained about withholding of blood transfusions from Aboriginal patients, inferior medicine chests required to be kept by employers of Aboriginal labour (compared with those at Royal Flying Doctor Service outposts), and legislation about Aboriginal people dying intestate.24-28 He was concerned that this legislation about the estates of Aboriginal people had been taken directly from the Mental Defectives Act: “The psychological trauma inflicted upon aborigines by regarding them and treating them as mental defectives and bankrupts must be immeasurable”.27 He similarly suggested that writers should avoid certain words, used by earlier conventions to describe Aboriginal people, that might inadvertently cause similar “psychological trauma” because of their negative metaphorical associations, or because he thought they were inaccurate or no longer acceptable.29 Christophers did not just promote positive over negative words and representations of Indigenous people, he investigated the portrayal of power in these representations and their colonial context. But no one questioned the fact that these representations of Indigenous people were created in their absence by non-Indigenous doctors. Enormous social changes since the 1950s in Australia make this omission seem obvious today. No longer can doctors expect to be unchallenged as the only authoritative voice on health matters. No longer can non-Indigenous people remain untroubled about the colonial context of their position when they speak about Indigenous people’s lives — or if they try to speak for Indigenous people. After the 1967 referendumFCAATSI’s 10-year campaign successfully led to 90.77% of voters in the 1967 referendum approving the deletion of the two discriminatory references to Indigenous people in the Constitution (Box 3). FCAATSI folded 10 years later after a decade of internal divisions concentrated on concerns about non-Indigenous control of the organisation.13 In part due to FCAATSI’s successes, attention had turned from equality to special Indigenous rights, like land rights, and Indigenous control of Indigenous lives. In the decades since the referendum, hundreds of Indigenous-controlled organisations, including health services, have been established and become successful. In more recent times, however, a new official and grassroots coalition promoting “reconciliation” between Indigenous and non-Indigenous Australians has emerged with prominent Indigenous and non-Indigenous leaders and members. While clearly lobbying in a different time and for different causes, this present-day coalition or social movement evokes memories of FCAATSI. This reconciliation movement has proved to be extraordinarily popular among both non-Indigenous and Indigenous Australians and very effective in spite of the considerable early and continued scepticism of many Indigenous people.30 With time, many people have forgotten or not heard of the activism and achievements of FCAATSI and its members like Barry Christophers. The dramatic changes in Indigenous lives and health that began in the 1950s and 1960s facilitated greater changes in the following decades. Joe McGinness, a Kungarakan man who lived in Cairns, was the President of FCAA (and FCAATSI) for most of its 20-year history. Christophers nominated him for the position in 1961 when he was first elected, and worked closely with him on many campaigns; they remained friends many years later. Sadly, Joe McGinness died in July last year. 1: Number of letters to the MJA editor about Indigenous health, 1914–1999 2: Barry Christophers in Melbourne, August 2000 Photograph: David P Thomas. 3: The Federal Council for Aboriginal Advancement (FCAA) and the 1967 referendum The first meeting of the FCAA declared its goal as equal civil rights for Aboriginal people (equal living conditions and pay and the removal of discriminatory legislation). In the 1960s, FCAA began to assert the need for different Indigenous rights (like land rights), not just equal civil rights.13,14 Torres Strait Islanders were acknowledged when the organisation changed its name to the Federal Council for the Advancement of Aborigines and Torres Strait Islanders (or FCAATSI) in 1964. Historian Peter Read has asserted that there were two dominant groups in the FCAA in its early years: the unions (and associated leftists, such as Christophers) and the churches. These groups included Aboriginal pastors like Doug Nicholls and Aboriginal unionists like Bert Groves and Joe McGinness, but these men had no special status as Indigenous people. FCAA and FCAATSI were “multi-racial” (or anti-racial) organisations, not Indigenous organisations — all people involved were treated “equally”—although, in practice, they were largely run by non-Indigenous people.13 The emphasis on the equality of Indigenous and non-Indigenous members reflected the organisations’ campaign goals for equal rights for Indigenous Australians. FCAATSI’s greatest public acclaim came with the success of its campaign for the 1967 referendum. The Australian Constitution had stated in Section 51 that the Commonwealth Parliament had the power to make “special laws” for the “people of any race, other than the aboriginal race in any State”. Section 127 stated that “aboriginal natives shall not be counted” in the populations of the states. While the referendum merely removed these two discriminatory references to Aboriginal people in the Constitution, FCAATSI’s campaign for the referendum was part of the larger social movement towards other, more significant equal rights. The referendum is now publicly and fondly (even though legalistically incorrectly) remembered for finally granting equal rights to Aborigines, including “citizenship” and the right to vote, as well as being associated with equal rights to drink alcohol.15

David P Thomas PhD, FAFPHM

Coeliac disease (CD) is caused by a complex immunological response provoked by grain protein in susceptible people. The majority of people with CD are symptom-free adults; the remainder are prone to a bewildering variety of signs and symptoms, ranging from infertility to type 1 diabetes. Many patients with undiagnosed CD spend years seeking help for complaints such as chronic tiredness or mild abdominal symptoms. In primary care, an appropriate target group to test for CD is people with anaemia (especially women), chronic tiredness, non-specific abdominal symptoms (including so-called “irritable bowel syndrome”), or a family history of CD. The response to an appropriate gluten-free diet is often life-transforming for symptomatic patients. Positive serological tests for CD require confirmation by duodenal biopsy and, if confirmed, referral to a dietitian and a coeliac society, followed by a life-long gluten-free diet.

John M Duggan MD, FRACP, FRCP

Setting You are a specialist in a teaching hospital. The unit is busy and you think there is a wealth of clinical material. You can’t seem to get the junior medical officers motivated to learn on the unit. They don’t seem interested in the discussions on the round. You’ve heard about building a good educational environment — but what does this mean? In the clinical setting we want to enhance the learning of students, junior doctors and trainees to help them be better doctors, but not increase the time we spend making that happen. Junior doctors are adults who want to learn. If we feel that learning is not progressing as it should, we need to consider whether the style in which we teach and the style in which junior doctors like to learn are matched and whether the clinical setting is conducive to learning. Adult learningAdult learning principles are not “evidence based”, but rather, as suggested by Malcolm Knowles, should be regarded as “models of assumption about learning”.1,2 If you ask yourself or the junior doctors to think back over what have been the best learning situations, and why, the following ideas are likely to surface: Personal motivation. Are junior doctors interested and eager to learn (internal motivation) or do they want to learn simply to pass an exam (external motivation)? Meaningful topic. Is the topic relevant to junior doctors’ current work or future plans? Have you made it clear why it is important? Experience-centred focus. Is learning linked to the work junior doctors are doing and based on the care they are giving patients? Appropriate level of knowledge. Is learning pitched at the correct level for junior doctors’ stage of training? Clear goals. Have you articulated the outcomes for the session/attachment/year so that everyone knows where you are heading? Active involvement. Do junior doctors have the opportunity to be actively involved in the learning process, to influence the outcomes and process? Regular feedback. Do junior doctors know how they are going? Have you told them what they are doing well, as well as what areas could be improved (positive critique)? Time for reflection. Have you given junior doctors time and encouragement to reflect on the subject and their performance (self-assessment)? Shifting from thinking about what you want to teach to what junior doctors want to learn (eg, asking what areas they are unclear about) shifts you from a teacher-centred to a learner-centred approach. Adults like to have an input into their learning Knowing the learnersLearning is about creating knowledge based on integrating new information with old, an active process that challenges the learner’s prior knowledge.3,4 As the learner progresses, there is often a shift from being dependent (where the learner needs substantial input and direction) to being interested (where the learner needs some guidance) to being self-directed (where the learner takes personal responsibility for his or her own learning). Our teaching style needs to take into account junior doctors’ prior knowledge and their stage of learning (Box).3,5 Expecting a struggling junior doctor to define his or her own needs, or presenting a mini-lecture to a mature and enquiring registrar, will demotivate both. Nevertheless, a degree of mismatch can challenge a learner and be a good thing. Shifting teaching styles from authoritarian (telling students what to learn) to delegating (getting them to tell us what they need to know) shifts the workload away from us and makes teaching and learning more fun. On the other hand, we all like to learn in different ways at different times — sometimes a didactic presentation is all we want. As teachers, we need to be flexible to suit the learners and the circumstances Educational environmentNot all “moments” in the clinical setting are good teaching moments, and to enhance the moments requires you to consider the following:5 Are the learners (or you) distracted by other duties, time constraints, tiredness, or hunger? Is the location busy, noisy, too public or uncomfortable? What is the atmosphere? Do the learners feel comfortable to demonstrate their lack of knowledge and ask questions or are they fearful of being humiliated? Do the learners feel as though they belong? Do they believe that their opinion is valued? Do the patients know what is expected? Have they agreed to be involved? Is their dignity respected? Take-home message In considering how to enhance learning in the clinical setting, ask yourself the following questions: Have I considered how junior doctors like to learn? What is my students’ motivation? Is the topic meaningful, pitched at the correct level and with clear goals? Is there active involvement, regular feedback, and time for reflection? Does my teaching style match my students’ learning stage? Is the environment supportive of learning? Matching learner stages to teaching styles3* Teacher styles Authority Motivator/ facilitator Delegator Learner stages Dependent learner Match Interested learner Match Self-directed learner Match * Adapted from Grow.4

Fiona R Lake MD, FRACP · Gerard Ryan MB BS, FRACP

Androgen deficiency is a clinical diagnosis confirmed by hormone assays. Among younger men, androgen deficiency is usually due to underlying hypothalamopituitary or testicular disorders. Androgen replacement therapy should be started after proof of androgen deficiency and should continue lifelong with monitoring. Men presenting with erectile dysfunction should be evaluated for androgen deficiency, but it is an uncommon cause; if overt androgen deficiency is confirmed, an underlying disorder needs further specialist investigation. In the absence of characteristic underlying testicular or pituitary disorders, new diagnosis of androgen deficiency in older men is difficult because of the non-specific symptoms and the decline in blood testosterone levels seen in healthy ageing and chronic medical disorders. There remains no convincing evidence that androgen therapy is either effective treatment or safe for older men unless they have frank androgen deficiency.

David J Handelsman FRACP, PhD · Jeffrey D Zajac PhD, FRACP

Leon A Flicker,* Samuel D Vasikaran,† Jenny Thomas,‡ John G Acres,§ Paul E Norman,¶ Konrad Jamrozik,** Nicola T Lautenschlager,†† Peter J Leedman,‡‡ Osvaldo P Almeida§§ * Professor of Geriatric Medicine, ‡ Research Nurse, School of Medicine and Pharmacology, § Research Fellow, School of Medicine and Pharmacology and School of Psychiatry and Clinical Neurosciences, ¶ Associate Professor of Surgery, †† Senior Lecturer in Psychiatry of Old Age, ‡‡ Professor of Medicine, §§ Professor of Psychiatry of Old Age; University of Western Australia, Royal Perth Hospital, Box X2213, Perth, WA 6000. † Head, Department of Core Clinical Pathology and Biochemistry, Royal Perth Hospital, Perth, WA. ** Professor of Primary Care Epidemiology, Imperial College London, London, UK. leonflicATcyllene.uwa.edu.au To the Editor: Elevated levels of homocysteine (Hcy) have recently been associated with increased risk of vascular events1 and dementia.2 The clearance of Hcy is dependent on three vitamins — folate, B6, and B12. Vitamin B12 deficiency has been described in older people for over 40 years,3 and may have wide-ranging effects through this vitamin’s influence on Hcy. The aims of this study were to examine serum B12 and folate status, and their relationships with plasma Hcy concentrations, in community-dwelling healthy older people living in Perth. Older men and women were recruited from two different sources: 299 men aged 75 years and over were recruited from a large population-based study of screening for abdominal aortic aneurysm,4 where 70% of those invited joined the project; and we recruited 273 community-dwelling women aged 70 years and over through advertisements. Exclusion criteria for both groups included significant cognitive impairment, severe physical illness and current use of B-group vitamin supplements. The Human Research Ethics Committee at the University of Western Australia approved the study, and all participants provided informed consent. Fasting total plasma Hcy, serum B12 and folate concentrations were measured in all participants, and serum creatinine concentration was measured in the men only to calculate glomerular filtration rate (cGFR). For analyses, the variable plasma Hcy was heavily skewed to the right and natural logarithmic transformation was used. Pearson’s product moment correlations were calculated for univariate analyses of continuous variables. Descriptive statistics are presented in Box 1. Fourteen per cent and 1% of the men, and 6% and 1% of the women, were deficient in B12 and folate, respectively. Hcy concentrations above upper reference limits (15 μmol/L for men and 13 μmol/L for women) were found in 24% of both men and women. There were significant (P < 0.001) positive correlations between age and log Hcy concentration for men (r = 0.23; 95% CI, 0.12–0.33) and women (r = 0.25; 95% CI, 0.13–0.36), inverse correlations between B12 and log Hcy concentrations for men (r = – 0.25; 95% CI, – 0.14 to – 0.35) and women (r = – 0.30; 95% CI, – 0.19 to – 0.41), and inverse correlations between folate and Hcy concentrations for men (r = – 0.43; 95% CI, – 0.33 to – 0.52) and women (r = – 0.28; 95% CI, – 0.16 to – 0.39). Plots of log Hcy against B12 and folate concentrations for all participants are presented in Box 2. Under multiple regression, the association of B12 and folate concentrations with log Hcy concentration remained after adjustment for age and cGFR in men only; beta values (SE) were: – 0.00060 (0.00011) for B12 concentration; – 0.0155 (0.0017) for folate concentration; – 0.0029 (0.0008) for cGFR; and 0.012 (0.005) for age. In this sample there were high prevalences of B12 deficiency and hyperhomocysteinaemia. Although the prevalence of folate deficiency was substantially lower, there were still moderate inverse associations between serum folate and Hcy concentrations. Unfortunately, vitamin B12 deficiency of this kind may not be universally corrected with small doses of oral supplements,5 and this has intensified concerns about precipitating neurological complications by population-based folate supplementation.6 There is a need for intervention studies of B-group supplements to evaluate whether the risks associated with hyperhomocysteinaemia can be ameliorated. 1: Demographic characteristics, serum B12 and folate, and plasma homocysteine in 299 older men and 273 older women Men Women Mean (SD) Range Mean (SD) Range Age (years) 78.9 (2.8) 68–86 74.8 (4.4) 70–92 Weight (kg) 78.4 (1.2) 50.6–119.5 69.3 (1.3) 39.0–120.0 Height (cm) 171 (6.5) 150–197 159 (6.7) 132–176 Body mass index (kg/m2) 26.6 (3.5) 16–37 27.4 (5.3) 17–52 Ever smoked 66% 41% Ever drank alcohol 95% 66% Serum folate (nmol/L) 24.3 (7.6) 5.5–45.3 (RI, 7–34) 25.3 (7.6) 3.9–45.2 (RI, 7–34) Serum B12 (pmol/L) 254.5 (116.7) 57–890 (RI, 140–646) 313.5 (158.7) 59–1270 (RI, 140–646) Plasma Hcy (μmol/L) 13.50 (5.3) 6.7–70.5 (RI, 6.0–15.0) 11.46 (6.8) 3.8–96 (RI, 5.0–13.0) Glomerular filtration rate (mL/min) 78.3 (16.3) 35.8–142.4 SD = standard deviation. Hcy = homocysteine. RI = reference interval. 2: Plot of serum B12 and folate concentration against log homocysteine concentration (with regression line for B12) in 299 older men and 273 older women

Leon A Flicker · Samuel D Vasikaran · Jenny Thomas · John G Acres · Paul E Norman · Konrad Jamrozik · Nicola T Lautenschlager · Peter J Leedman · Osvaldo P Almeida

Malcolm H Parker Associate Professor of Medical Ethics, School of Medicine, University of Queensland, Herston Road, Herston, QLD 4006. m.parkerATuq.edu.au To the Editor: Gerber1 appears sympathetic to the following reasons for rejecting damages in cases of wrongful birth, quoted from the High Court minority in Cattanach v Melchior,2 and judges in similar cases: doctors do not owe a duty of care that protects the economic interests of patients; the birth of a healthy child should not be regarded as a legal harm, because the birth of a healthy child is a good thing, the cost of rearing a child does not exceed the value of parenthood, and parents ought not to enjoy the advantages of parenthood without the concomitant responsibilities; awarding damages would indicate to the child that he or she was unwanted; and doctors should not be liable for most of the costs of rearing a child, because parents have a choice of rearing the child or surrendering it for adoption. As to the first point, why should doctors be exempt from any loss that results from their negligence? Depicting this duty as one of “protecting economic interests” distorts the nature of the duty of care, which requires the duty holder to avoid foreseeable damage, which includes economic loss consequent on the negligence. Regarding the second point, balancing the costs of rearing the child against the value and advantages of parenthood is conceptually misleading. The implication is that the value of parenthood should render the costs of rearing the child relatively trivial. A more coherent interpretation is that, because the costs of rearing the child and the value of parenthood are incommensurable, the natural love for the child and the value of parenting that follow the birth ought not discount the damage. This interpretation also informs responses to the third and fourth points. Not wanting another child, and not wanting the particular child once it exists, are distinct concepts. The idea that Jordan Melchior was not wanted at the time his parents took steps to avoid further pregnancies is incoherent. Wanting to avoid further pregnancies and wanting to nurture the child who is born are perfectly consistent positions, whether the case involves forgotten contraception or negligent sterilisation. Finally, the idea that, because they have the choice to keep or surrender the child, the parents should bear the costs if they keep it suggests that, once born, the particular child can be regarded as a commodity — something that the general position against awarding damages for wrongful birth repeatedly disavows. One of the judges quoted by Gerber claimed that such children would come to think of themselves as unwanted, and that this was “obscene”. The same judge’s glib claim that the parents can choose to keep or surrender the child strikes me as the obscenity.

Malcolm H Parker

Paul Gerber Honorary Reader in Legal Medicine, University of Queensland, Brisbane, QLD. In reply: Parker’s letter does little more than repeat the arguments that found favour with the majority in the High Court. He approaches the issues raised by this controversial litigation from an ethical perspective. Alas, the parents’ claim for the cost of raising a healthy child, conceived as a result of the alleged negligence of the defendant gynaecologist, raises the legal issue of restitution: does the law of tort recognise this head of damages as a “loss” for which parents may be compensated? Courts have, in the past, answered this question by reference to general principles based upon legal values. In the Melchior case,1 the majority departed from that hallowed principle. So be it. Does that make Jordan Melchior a “commodity”, having a commercial value? Yes! The plaintiffs faced the choice of either keeping their son, or mitigating their “loss” by placing him for adoption. They chose the former. Priestley JA had, in an earlier case, put the issue succinctly: “After that decision was made, the defendant was not legally responsible for the parents’ financial cost of rearing the child”2 (this was restated by Kirby J in the Melchior case1). Parker may not like it, but the law of tort has — up till now — shown more caution in awarding damages for what is called pure economic loss (ie, loss affecting purely financial interests) than it has in relation to conduct that causes damage to person or property. Before the Melchior case, that distinction had been firmly embedded in the law of tort and formed the basis of established rules governing liability for damages.3 That distinction has now been blurred by placing a financial value on the parent–child relationship.

Paul Gerber

Bronwyn A L Crawford,* Channa Perera† * Endocrinologist and Clinical Senior Lecturer, Royal Prince Alfred Hospital and the University of Sydney, Sydney, NSW 2050; † Endocrinologist, Orange Base Hospital, Orange. brcrawfoATmail.usyd.edu.au To the Editor: Prolonged hypoglycaemia in patients taking a sulfonylurea may be refractory to intravenous glucose treatment with fatal consequences, as described by Veitch and Clifton-Bligh.1 Although these authors briefly mention the use of octreotide, we believe that an additional point in the “Lessons from practice” should have been: Octreotide may be an effective therapy in refractory sulfonylurea-induced hypoglycaemia. We describe the first two patients in whom we used this therapy. A 76-year-old man with type 2 diabetes was admitted after an acute myocardial infarction and cardiac arrest. He was successfully resuscitated and underwent emergency bypass surgery. His diabetes was controlled with gliclazide 80 mg twice a day. After surgery, he developed cardiac failure, renal impairment (serum creatinine level, 0.22 mmol/L) and frequent hypoglycaemic episodes. The gliclazide was stopped but, despite good oral dietary intake, hypoglycaemia worsened and failed to respond to vigorous intravenous glucose therapy. He suffered a hypoglycaemic seizure (blood sugar level, 0.8 mmol/L). Over the next day, he received more than 300 g of glucose in the form of a 10% glucose intravenous infusion, but, despite this, went into hypoglycaemic coma. Blood results were: insulin, 472 pmol/L (reference range [RR], 15–60 pmol/L); C-peptide, 7616 pmol/L (RR, 300–800 pmol/L); and gliclazide, 9.4 mg/L (steady state average, 2.5 mg/L). He was given an intravenous infusion (30 ng/kg per minute) of octreotide.2 Within an hour, his blood sugar level rose to 7.9 mmol/L and continued to rise. Dextrose and octreotide infusions were ceased within 13 hours, with no further episodes of hypoglycaemia. He was discharged home 2 days later. A 75-year-old man with type 2 diabetes was taking glibenclamide 2.5 mg each morning. He was transferred from a rural hospital with acute on chronic renal failure (serum creatinine level, 0.4 mmol/L), as well as recurrent hypoglycaemia. The glibenclamide was stopped, but blood sugar levels remained low, and he became comatose despite boluses of 50% dextrose and a continuous infusion of 10% dextrose. The high volume of intravenous fluid precipitated cardiac failure and pulmonary oedema, requiring inotropic support. Blood results were: blood sugar, 1.5 mmol/L; insulin, 1250 pmol/L; C-peptide, 20 949 pmol/L. As an alternative to the high-dose, continuous infusion of octreotide used in our first patient, we administered a single subcutaneous injection of octreotide 50 μg. One hour later, the patient’s blood sugar level had risen to 9.0 mmol/L. He had no further episodes of hypoglycaemia. Eight hours later, insulin and C-peptide levels had fallen markedly (insulin, 153 pmol/L; C-peptide, 5654 pmol/L). He made a full recovery. Octreotide is a somatostatin analogue that inhibits the secretion of a number of neuropeptides, including insulin. It is a safe and effective therapy for sulfonylurea-induced hypoglycaemia when initial therapy with oral or intravenous glucose fails.2-5 It is particularly useful in elderly patients with renal or cardiac complications, in whom fluid overload may be a limiting factor in intravenous dextrose therapy. Octreotide may also break the vicious circle that can occur in sulfonylurea-induced hypoglycaemia in which repeated dextrose boluses further stimulate insulin release.

Bronwyn A L Crawford · Channa Perera

Peter C Veitch,* Rory J Clifton-Bligh† *Specialist in Geriatric Medicine, Department of Aged Care and Rehabilitation Medicine; † Registrar in Endocrinology, Department of Endocrinology, Royal North Shore Hospital, Clinic 1, Level 3, Pacific Highway, St Leonards, NSW 2065. rcliftonATmed.usyd.edu.au In reply: Crawford and Perera highlight a very important point with respect to hospital-based treatment of sulfonylurea-induced hypoglycaemia. Whereas, in our article,1 we wished to emphasise the importance of recognising and preventing this condition in primary care settings, we agree that octreotide is an effective therapy in treating this condition. Octreotide inhibits the specific effect of sulfonylureas (glucose-stimulated β-cell insulin release) and prevents rebound hypoglycaemia, which, in this situation, may occur with the use of glucose.2 Case reports, including those elegantly presented and referenced by Crawford and Perera, clearly illustrate the safety and efficacy of octreotide in treating sulfonylurea toxicity when initial therapy with glucose fails. Octreotide may be administered either intravenously or subcutaneously, and its effect is maintained after a short course of therapy. At our own institution, we have now adopted guidelines for the treatment of refractory sulfonylurea-induced hypoglycaemia, which include the administration of octreotide (50 μg subcutaneously) every 8 hours for up to three doses, although, as Crawford and Perera note, some patients will have a sustained response after a single dose.

Peter C Veitch · Rory J Clifton-Bligh

Malvinder S Parmar Medical Director (Internal Medicine), Timmins and District Hospital, Suite 108, 707 Ross Ave East, Timmins, ON P4N 8R1, Canada. atbeatATntl.sympatico.ca To the Editor: I wish to add another cause of exogenous hyperthyroidism to those mentioned in the comprehensive review on hyper- and hypothyroidism by Topliss and Eastman.1 Inadvertent ingestion of animal thyroid (“hamburger” thyrotoxicosis), although rare, is worth mentioning. Meat may be inadvertently contaminated with thyroid tissue through the process of “gullet trimming” during butchering. While this process has been prohibited in most countries since the recognition of outbreaks of hamburger thyrotoxicosis,2,3 it may still occur when farm animals or wild game are prepared for consumption by farmers, hunters or local butchers unaware of the prohibition. I recently reported a case of a woman living on a farm in Canada who had five episodes of transient hyperthyroidism over a decade.4 These were initially diagnosed as episodes of “silent thyroiditis”, but were later attributed to consumption of meat patties contaminated with thyroid tissue, as the local butcher was not aware of the prohibition on gullet trimming. A history of eating wild game or locally prepared meat should be considered before a diagnosis of silent thyroiditis is made. Thyroid uptake of radioiodine is low in both conditions, but serum thyroglobulin level is raised in thyroiditis and decreased during the hyperthyroid phase of exogenous hyperthyroidism.

Malvinder S Parmar

Ngaire T Jones Medical Practitioner, Beaconsfield, WA. ngairejATbigpond.com To the Editor: The recent article on thyroid disorders by Topliss and Eastman notes that “around the world, iodine deficiency still remains the predominant cause of hypothyroidism” and furthermore that “mild iodine deficiency is re-emerging in Australia”.1 Indeed, the Journal has recently published at least two articles suggesting that the iodine status of the Australian population needs to be further explored.2,3 My question therefore is: when treating a patient who has results indicating clinical or subclinical hypothyroidism, would it be relevant and important to test for iodine deficiency (by 24-hour urine collection)? This seems analogous to undertaking iron studies in a patient with a falling haemoglobin level. In the same way that iron deficiency can exist and produce symptoms, even in the absence of anaemia, may not iodine deficiency affect health and well-being? Without the elemental “building blocks” of iron and iodine, the relevant systems are put into overdrive to no avail. It seems simple to test routinely for this possibility, correct any deficiency and then recheck thyroid function. There may be more “clinically significant iodine deficiency” than we realise. As it will no doubt be some time until further studies in the Australian population shed more light on this, is it not relevant meanwhile to at least check for this possibility in individual patients?

Ngaire T Jones

Duncan J Topliss,* Creswell J Eastman† * Director, Endocrinology and Diabetes, Alfred Hospital, Commercial Road, Melbourne, VIC 3004; † Director, Institute of Clinical Pathology and Medical Research, Westmead Hospital, Sydney, NSW. Duncan.toplissATmed.monash.edu.au In reply: Jones asks if iodine excretion should be measured routinely in all patients with hypothyroidism in Australia as part of the initial assessment. We do not advocate this for the following reasons. Urinary iodine estimations are unreliable for assessing individual patients, as urinary iodine levels can vary considerably from day to day with iodine intake. These measurements should be reserved for population studies to provide an overall assessment of iodine nutrition in that population. In Australia, it is probable that virtually all cases of primary hypothyroidism are caused by chronic autoimmune lymphocytic thyroiditis, ablative therapy for Graves’ disease, or inadequate thyroxine replacement therapy in these conditions, as is the case in the United States and the United Kingdom.1-3 This contention is supported by data from the Busselton (Western Australia) survey on thyroid peroxidase antibody levels,4 which suggest that these antibodies will be of great diagnostic assistance, in contrast to the dubious clinical value of individual measurement of iodine excretion. In support of this view, in a large survey of the US population, where iodine intake has probably fallen similarly but not to the same degree as in Australia, there was no association between low urinary iodine levels and increased serum levels of thyroid stimulating hormone (TSH).5 In that study, the significant association between raised TSH and female sex disappeared after controlling for the presence of thyroid peroxidase antibodies, while the prevalence of clinical hypothyroidism was strongly correlated with positive results for these antibodies. In Australia, current information indicates that iodine deficiency, where it exists, is mild. The prevalence and regional variation are currently the subject of the National Iodine Nutrition Survey, which is surveying iodine excretion and thyroid size in primary school children. There is no evidence that this mild deficiency is associated with an increased prevalence of hypothyroidism. Jones’s suggestion that iodine deficiency impairs health by a mechanism other than impairment of thyroid function is not supported by any scientific evidence. Any consideration of advocating routine assessment of iodine status should await the results of the ongoing national study. However, iodine nutrition would appear to be best addressed as a public health issue, by promoting use of iodised salt and ensuring adequate iodine nutrition in pregnant and breastfeeding women and their infants.

Duncan J Topliss · Creswell J Eastman

David S Elder Occupational Physician, 517 St Kilda Road, Melbourne, VIC 3004. delderATbigpond.net.au To the Editor: In Bogduk’s review of the management of low back pain,1 he cited several international guidelines but did not address the effect of returning the patient to work. Disappointingly, return to work was mentioned only as an outcome of multidisciplinary therapy, with no mention at all of a planned and purposeful return to work in the suggested approach. This is surprising, given the literature available2,3 and the significant adverse effects of being out of work.4 Further, the algorithm in Box 3 (general practice management of chronic low back pain) appears to have a never-ending loop: I am cautious of the adverse effects that the reductionist model can have,5 and it appears possible in this algorithm to be forever stuck in the investigative loop. An additional pathway from this loop to intensive therapy would allow progression in some cases. The inclusion of a return to work in management of low back pain has been extensively analysed in the Australian setting and shown to significantly reduce disability.6 This advice should be included in any clinical update on management of low back pain.

David S Elder

John Salmon,* Anna Hilyard† * Pain Management Specialist, Bethesda Hospital, 25 Queen Mary Drive, Claremont, WA 6010; † Director, Achieve Pain Control Group, Perth, WA. salmon8ATbigpond.com To the Editor: Bogduk’s article on management of chronic low back pain1 was disappointingly retrogressive as a guide for general practitioners. Compartmentalising back pain management as monotherapy, multidisciplinary therapy or “reductionism”, and favouring the last, reinforces the medical model which has singularly failed to stem the epidemic of low back pain disability affecting the developed world. The biopsychosocial model of chronic spinal pain is now widely accepted and rationally emphasises the multi- or interdisciplinary model of management.2,3 Bogduk’s preference for the reductionist approach may be reasonable in a specialised centre and as a basis for research, but must justify its practical relevance in the face of the following: Available data on the reductionism approach are meagre, conflicting and mainly derived from pain-clinic populations likely to differ from patients presenting to GPs. Diagnostic joint and disc injection procedures and radiofrequency treatment performed to the required standard are available in only a very few centres. Radiofrequency lesioning of the nerve supply to symptomatic joints has been shown to provide pain relief limited to 9–18 months.4 Repeat lesioning may be less effective and is impracticable in the long term. At best, these treatments could be considered palliative. Of course, patients can only benefit from accurate diagnosis and reduction of pain from identified peripheral generators. Unfortunately, for most people with chronic back pain, it is not that simple. Usually there are multiple pathologies and pain generators, multisegmental dysfunction, disrupted motor control and interacting peripheral and central neural sensitisation mechanisms. And that is just the “bio” of the biopsychosocial model. There is then the interplay with the individual’s psychological and social environment. It is often a challenge to communicate the diagnosis effectively in the face of conflicting input from other health providers, the media and patient preconceptions. Just “plonking” “the diagnosis” before a patient and dangling a seductive “techno fix” that does not deliver in the long term is precisely what renders patients with chronic pain increasingly bewildered, dysfunctional and desperate to try one passive treatment after another. The biopsychosocial model provides a basis for management in both general and specialist practice. Appropriate interventions to reduce pain-generator input are embedded in a cognitive behavioural management matrix that imbues patients with accurate, relevant knowledge of their conditions and commonsense self-management techniques to maintain appropriate activity levels, goal setting and psychological positivity. For a time-challenged GP, collaboration with an activation- and exercise-oriented physiotherapist can be effective. The GP’s role is to provide the “white coat authority” so vital in recruiting patient confidence.

John Salmon · Anna Hilyard

Nikolai Bogduk Director, Department of Clinical Research, Royal Newcastle Hospital, Newcastle, NSW 2300. mgillamATmail.newcastle.edu.au In reply: There is a difference between wishful thinking and evidence. Elder advocates a focus on return to work. Elsewhere, I have described how this should be pursued.1 However, the evidence supports success only in the context of acute and subacute pain. I was commissioned to write on low back pain. In that context, evidence is lacking. Even Waddell, whom Elder cites,2 conspicuously avoided the issue of chronic low back pain; his evidence pertains only to acute low back pain. Salmon and Hilyard promote the biopsychosocial model. Indeed, this model is now widely accepted. Even our own studies have shown how successful it can be to recognise and treat patients’ fears and mistaken beliefs.3 However, the evidence of success is limited to acute and subacute low back pain. The predictions of the biopsychosocial model have not been fulfilled in the context of chronic low back pain. Although better than no therapy, behavioural therapy is not more effective than other therapies, and does not “reduce pain generator input”, as Salmon and Hilyard contend. Insurers, who pay for this treatment, do not share their enthusiasm for it.4 Salmon and Hilyard also repeat the commonly held view that patients have multiple pain generators. There is no actual evidence for this assertion, while the available evidence indicates the opposite. When investigated comprehensively, fewer than 10% of patients have more than one simultaneous pain generator.5 Further, Salmon and Hilyard consider that complete relief of pain for 9–18 months amounts to palliative therapy. Yet the opposite is true. Not relieving pain by behavioural therapy is palliative. They also deprecate radiofrequency neurotomy with the accusation that it “may be less effective” when repeated, but fail to cite the literature showing that this is not the case. They are correct in stating that reductionist procedures performed to the required standard are available in only a few centres. However, this does not invalidate these procedures; it reflects only a political and ideological problem in healthcare delivery. They also fail to reveal that in many places where these procedures are available, they are not performed according to best-practice standards. It is not the procedures, but misguided and unscrupulous practitioners, who render patients bewildered and dysfunctional.

Nikolai Bogduk

Gordon Broderick Executive Director, Distilled Spirits Industry Council of Australia, 1st Floor, 117 Ferrars Street, South Melbourne, VIC 3205. gordonbATdsica.com.au To the Editor: In their article on risk-taking behaviour among young Australian women, Carr-Gregg and colleagues make a number of statements about alcohol consumption among young women.1 Unfortunately, these statements are not supported by the facts. The authors assert, citing a national study of 14 762 women aged 18–23 years,2 that “seventy percent of young women engage in ‘binge drinking’ (5 or more drinks on one occasion) at some time, with 19% doing so on a weekly basis”. The level and frequency of alcohol consumption that constitutes “binge drinking” is a matter of conjecture. The National Health and Medical Research Council (NHMRC), in guidelines released in 2001,3 state that “binge drinking” is “not a preferred term due to its lack of consistent and specific meaning”. The NHMRC guidelines on short term risk specify 5–6 alcoholic drinks for a female on any one day as being “risky” for health, and 7 drinks or more being “high risk”. For long term risk, 3–4 drinks on an average day, or 15–28 drinks a week, is considered “risky”, with any more constituting “high risk”. Applying these guidelines to the Women’s Health Australia dataset shows that 5.1% of young women engage in drinking that is “risky” or “high risk” in the long term. Of the remaining 94.9%, 14.4% drink 5 or more drinks weekly or more, and 51.9% drink five or more drinks monthly or less. This is a more revealing (and accurate) picture than the blanket statement that “70% of young women are ‘binge drinkers’ ”. Carr-Gregg and colleagues also claim that “22% of females aged 14–19 years drink between 9 and 30 alcoholic drinks a day”. The source for this statement is a survey conducted for the Salvation Army.4 The survey has several limitations, not least the small sample size. The survey sampled 614 respondents, of whom 70 were aged 14–19 years. The assertion that 22% of females in this age category were “binge drinkers” is based on just seven respondents. This number is well below what is required for any reliable statistical estimation. Encouraging responsible drinking among younger people is a major goal of health professionals and the alcohol industry. A constructive policy debate on this issue requires sound, objective evidence about alcohol consumption among younger people. The article by Carr-Gregg et al does not represent progress towards providing that evidence.

Gordon Broderick

A nasogastric feeding tube became acutely blocked in a young woman with anorexia nervosa. The ward staff tried unsuccessfully to remove the tube, and the patient complained of left cheek and nose pain. The knotted tube had impacted in the nose and was subsequently removed under anaesthesia. Whether the knotting was with fingers or tongue is unknown.

Desmond Wee MB BS · Jon P Clarke MBChB, FANZCA

Constructing RSI: Belief and desire. Yolande Lucire. Sydney: UNSW Press, 2003 (xvi + 216 pp). ISBN 0 86840 778 X. It is with some interest that this reviewer, a clinical and investigative rheumatologist who is too young to have experienced the height of the repetitive strain injury (RSI) epidemic, finds himself being asked by the Medical Journal of Australia to report on independent medical examiner and forensic psychiatrist Yolande Lucire’s popularisation of her 1996 PhD thesis. Dr Lucire was a significant critic during the 1980s epidemic and still believes that the Medical Journal of Australia should have withdrawn several of the articles it published, and through which it irresponsibly contributed to the epidemic. It is clear that attitudes remain acrimonious and polarised on these matters. Dr Lucire continues in her view, even in the “endemic” period of recent years, that RSI is entirely a psychogenic disorder due to somatisation of psychosocial distress. As evidence, she relates the results of her PhD. This was a retrospective case study review of 100 (out of 319) randomly selected RSI patients who had been referred to her for an opinion between 1984 and 1991. She used census statistics for controls, and found that virtually all the patients had one or more personal problems or disruptive life events close to the time of seeking compensation. She also impressively reviews the historical forces of the time, highlighting the lack of correlation between workload and symptoms, and the persistent absence of objective abnormalities. Hers may have indeed been the most robust investigation of the RSI phenomenon possible for the epidemic, but it is tragic that no serious follow-up study of RSI sufferers has ever been performed. Moreover, a diligent Medline search will reveal more recent contrary epidemiological data and growing evidence for peripheral and central neural changes, at least some of which might not be reversible. The jury remains out as to whether RSI is just somatisation. Richard A KwiatekRheumatologist Queen Elizabeth HospitalAdelaide, SA

Richard A Kwiatek

Blood and guts: a short history of medicine. Roy Porter. New York: W W Norton, 2002 (199 pp). ISBN 0 393 03762 2. Roy Porter may have left this earth prematurely, but this most productive of modern scholars had some of his best books still in the publisher’s pipeline and he continues to delight and surprise us. Formerly Professor in the Social History of Medicine at the Wellcome Trust in London, Porter brings the outstanding scholarship of our time to the general reader. His vivid narrative enlightens and invites us to reflect on the large questions that medicine and care of the sick pose for a civilised society. He begins with a history of human disease, what he calls that “war between disease and doctors fought out on the battleground of the flesh” that has “a beginning, a middle and no end”. We are reminded that most disease is of our own making, an unwitting product of our drive to farm, irrigate, domesticate herd animals, live in towns and cities, travel, conquer and colonise. Likewise, our determination to extend our mortal coil demands a price in chronic illness, disability and dementia. Chapters discuss, in turn, doctors, the body, the laboratory, therapies, surgery and the hospital, each exploring its theme with a long historical view from ancient to modern. There is no more lucid guide to Hippocrates, Galen, the Scientific Revolution and the Paris Clinic to be found. The final chapter on medicine in modern society reviews the transition from the private relationship between patient and healer to a healthcare industry that is integral to the machinery of an industrialised society. Yet, for all biomedicine’s achievements, the health of the world’s poor has scarcely improved, while the “worried well” of the West consume a disproportionate amount of the available health dollar. Thus at the beginning of the 21st century, after “a golden age of some generations back, the public climate is not one of optimism but of new-millennial anxiety.” Janet S McCalmanReader in History Johnstone-Need Medical History Unit University of Melbourne, VIC

Janet S McCalman

Manual of travel medicine and health. 2nd ed. Robert Seffen, Herbert L DuPont, Annelies Wilder-Smith. Hamilton, ONT: B C Decker, 2003 (xii + 628 pp + CDROM). ISBN 1 55009 227 8. This easy-to-read, pocket-sized edition of the Manual of travel medicine and health is written by two past presidents and founding directors of the International Society of Travel Medicine (Herbert DuPont and Robert Steffen) and a practising clinician (Annelies Wilder-Smith). The authors have considerable experience in epidemiology, research and clinical medicine, as well as many years teaching travel medicine, and this experience shows. Like the first edition, this book focuses on the more common travel health problems. There is more information on special-risk groups such as senior travellers, pregnant women, children and the immunocompromised, and new sections on bioterrorism and migration medicine. Information on deep vein thrombosis and pulmonary embolus, as it relates to travel, has been updated. There is a very useful, short bibliography after most sections and many of the articles are from the authoritative Journal of travel medicine. The book is organised in a logical reading manner and the authors obviously understand the needs of the practitioner working at the clinical coalface. In general, the information is well presented and educative rather than “cookbook” style, and the authors are constantly reinforcing the message that many travel health problems, such as foodborne and waterborne diseases and insectborne diseases, cannot be prevented by vaccination. The section on the major infectious diseases includes a brief paragraph on “Risk to travellers” for each disease which puts the real risk into perspective. The major topics of malaria and traveller’s diarrhoea are dealt with in depth. Common non-infectious health risks and their prevention are discussed. Topics include jet lag, altitude sickness, motion sickness and diving medicine. There is also brief coverage of the health problems of the returned traveller. In a book of this size it would be impossible to cover this fully; however, the major concerns — fever, persistent diarrhoea, eosinophilia and sexually transmitted diseases — are all included. In summary, the Manual of travel medicine and health, as a resource for travel medicine physicians, is as good as one can find in a book of this size. A quality assurance audit on any travel medicine practice should check whether this book is present on the bookshelf. Robert B KassChief Medical Advisor The Travel Doctor Group (TMVC) Adelaide, SA

Robert B Kass

Woman performs own caesar A 40-year-old multiparous woman, with a previous obstetric history of death- in-utero, took drastic action when she found herself unable to deliver her ninth pregnancy vaginally at home, say the mostly Mexican authors of a case report. After taking three glasses of “hard liquor”, the woman used a kitchen knife in three attempts to slice her abdomen in the right paramedial region and cut her uterus longitudinally to deliver a male infant. Another of her children summoned help; a local nurse arrived to find the mother unconscious and eviscerated. The woman survived the ordeal, which included an 8-hour car trip to the nearest hospital and two exploratory laparotomies, as did her infant. The family live in a small village deprived of running water, electricity and sanitation, as well as prenatal care. Int J Gynaecol Obstet 2004; 84: 287-290 Pre-hospital adverse events Researchers studying adverse events in patients admitted to a Canadian teaching hospital have called for quality-improvement efforts in ambulatory care. The Ottawa Hospital Patient Safety Study identified 64 patients with adverse events in a randomly selected sample of 502 adult hospital patients. Three in five events occurred before admission, and half of these occurred in an ambulatory setting — in the patient’s home or nursing home or a doctor’s offices. Adverse events of this type were almost always adverse drug events and were often preventable, the researchers said. CMAJ 2004; 170: 1235-1240 Intensive lipid lowering A group of international researchers has suggested that target low-density lipoprotein (LDL) cholesterol levels for secondary prevention may need to be lowered even further in light of new findings. PROVE IT — the Pravastatin or Atorvastatin Evaluation and Infection Therapy trial, conducted in 4162 patients in eight countries — has shown intensive statin therapy (80 mg atorvastatin daily) to be superior to standard therapy (40 mg pravastatin daily) in terms of major cardiovascular deaths in the first few years after either acute myocardial infarction or high-risk unstable angina. However, there were more liver-related side effects with high-dose atorvastatin than with standard-dose pravastatin. The mean LDL cholesterol level in the atorvastatin group was 1.6 mmol/L. N Engl J Med 2004; 350: 1495-1504 “Lids for Kids” Community agencies wanting to reduce both childhood injuries and socioeconomic inequalities should consider providing free bicycle helmets together with an educational pack, say UK researchers. These measures increased not only helmet ownership but also helmet use in their trial involving more than a thousand nine- and 10-year-old schoolchildren from nearly 30 primary schools in deprived areas of Nottingham. Arch Dis Child 2004; 89: 330-335 Professional misconduct A doctor practising complementary medicine has been removed from the Register of Medical Practitioners in New Zealand for professional misconduct — among other things, the doctor was found to have made untenable diagnoses via undue reliance on an implausible technique (peak muscle resistance testing) to the exclusion of conventional medical diagnostic methods and when not supported by the clinical presentation. A report of the NZ Medical Practitioners Disciplinary Tribunal’s decisions said there is an onus on doctors who practise alternative or complementary medicine to inform patients not only of the nature of the alternative medicine offered, but also the extent to which it is consistent with conventional theories of medicine and has, or does not have, the support of the majority of practitioners. “Patients consult them [doctors] to get the ‘best of both worlds’ and to avoid those aspects of alternative medicine which are extreme or incredible,” the report said. www.nzma.org.nz/journal/ 117-1191/825/ Antidepressants in youth Antidepressant drugs cannot confidently be recommended as a treatment option, let alone as first-line treatment, for depression in childhood and adolescence, according to Australian authors. Jureidini and colleagues had reviewed six published randomised controlled trials involving newer antidepressant agents such as selective serotonin reuptake inhibitors and venlafaxine. They said that study investigators’ conclusions exaggerated the benefits and downplayed the adverse effects of such treatment. BMJ 2004; 328: 879-883 — Dr Ann Gregory, MJA

Ann Gregory

Med J Aust 2004; 180 (10 Suppl).