Letters

In reply: The main conclusion of our population-based study1 was that a consistent increase in bicycle-related injuries occurred over the study period. Our study was not designed to analyse the effect of helmet wearing. The potential benefits of helmet wearing were identified in the discussion as a means of reducing the increasing burden of injury. There has been opposition to legislation enforcing helmet wearing in Australia.2 The response to this opposition has been adequately addressed by Canadian researchers.3,4 In addition, a number of Cochrane systematic reviews have arrived at different conclusions to Wardlaw.5,6 Although there are no randomised controlled trials, the weight of evidence would suggest that wearing helmets reduces head injuries in the bicycle-riding population and the imposition is worth the inconvenience to bicycle riders.

Antonina A Mikocka-Walus · Francis T McDermott · Peter A Cameron

To the Editor: Following the letter by Kitson et al, about a patient with asymptomatic ocular syphilis,1 we describe another unusual presentation of syphilis, with perioptic neuritis that mimicked papilloedema. A 28-year-old man presented with blurry central vision of his right eye on waking. He had had flu-like symptoms 2 days before presentation. There were no symptoms suggestive of meningitis, no raised intracranial pressure and no obvious ocular infection or inflammation. He had been diagnosed with type 2 diabetes mellitus at age 15 years, and had no known microvascular complications. His only medication was metformin. His visual acuity was 6/12 in the right eye and 6/6 in the left. The right eye had an enlarged blind spot with a small paracentral scotoma, with a central relative scotoma to red. The visual field in the left eye was normal. There was no relative afferent pupillary defect, and the anterior chambers were normal. Fundoscopy confirmed bilateral swelling of the optic discs (Box). Computed tomography and magnetic resonance imaging of the brain excluded space-occupying lesions and demyelination. Examination of the cerebrospinal fluid (CSF) showed: normal opening pressure; a white cell count of 66 × 109/L (reference range, 4–11 × 109/L), 100% lymphocytes; a protein concentration of 1.12 g/L (reference range, 0.15–0.45 g/L); a glucose concentration of 8.9 mmol/L (reference range, 2.7–4.4 mmol/L); and no bacterial growth. Findings of a baseline blood analysis were normal, but with an elevated glycated haemoglobin (HbA1c) level of 10.5% (reference range, < 6%), indicating poorly controlled diabetes. We thus initially considered diabetic papillopathy and non-arteritic ischaemic optic neuropathy, but the patient subsequently (about a week later, after most other investigations gave negative results) reported having had unprotected sexual intercourse with different men about 5 months previously. He recalled having a transient palmar maculopapular rash 2 months before presentation. Neurosyphilis was then confirmed with a strongly positive result on an absorbed fluorescent treponemal antibody (FTA-ABS) test in CSF. Results of serological tests for syphilis were positive (reactive [3+] on a Treponema pallidum particle agglutination test and a markedly elevated titre on a rapid plasma reagin test [1:128]), but results of tests for HIV and hepatitis were negative. Contact tracing was initiated. After 21 days of treatment with intravenous penicillin, the vision in his right eye was completely restored. At 9-month follow-up, the bilateral swelling in his optic discs had resolved, and there was a tenfold decline in the rapid plasma reagin test titre (1:8). This case illustrates syphilitic perioptic neuritis with optic disc swelling that is indistinguishable from papilloedema. Perioptic neuritis describes inflammatory involvement of the optic nerve sheath without inflammation of the nerve itself. The affected eye often has normal visual acuity with no visual field defect except for an enlarged blind spot.2,3 The prevalence of infectious syphilis has been rising in recent years, especially in Victoria and New South Wales, predominantly among men who have sex with men.4,5 Endemic syphilis should also be considered in patients with HIV co-infection and Indigenous patients, particularly those in the remote communities of Western Australia. Physicians should be vigilant in looking for neurosyphilis in any sexually active individual with unexplained eye or neurological signs. The swollen optic discs of a patient with syphilitic perioptic neuritis

Grace S H Low · Robert H Edis

To the Editor: We report a case of a 13-year-old girl with cystic fibrosis (CF) and chronic Pseudomonas aeruginosa lung infection who developed an unusual infection that was challenging to manage. At a regular review, and with no obvious change in clinical respiratory status, the patient’s forced expiratory volume in 1 second (FEV1) was 70% of the predicted value — a drop from her usual 90%. A subsequent 3-week admission, including treatment with standard antipseudomonal antibiotics, physiotherapy and addition of nebulised dornase alfa, did not significantly improve her lung function. She was discharged home on a trial of azithromycin. One month later, she had a non-productive cough, and a bronchoalveolar lavage specimen showed no growth on culture. Four months later, the patient presented with increased non-productive cough and sudden further deterioration in FEV1 to 52% of the predicted value. She was admitted and given standard intravenous antipseudomonal antibiotics. Culture of a repeat bronchoalveolar lavage specimen grew Mycobacterium abscessus, sensitive to clarithromycin, imipenem and amikacin; hence, the patient was given intravenous imipenem and amikacin for 3 weeks. During this period, high-resolution computed tomography (CT) of the patient’s chest showed mucus plugging, marked diffuse parenchymal involvement with typical “tree-in-bud” appearance and, surprisingly, given her poor lung function, only moderate bronchiectasis (Box). Two years earlier, results of a chest CT scan were normal. The patient was discharged home on long-term nebulised amikacin, oral ciprofloxacin and oral clarithromycin. Her lung function gradually improved after discharge and, 6 months later, her FEV1 was 69% of the predicted value and a sputum culture produced no growth. CF is a risk factor for non-tuberculous mycobacterial (NTM) lung disease, which is notoriously difficult to eradicate. A recent multicentre prospective study in the United States estimated that, in patients with CF who are older than 10 years, the prevalence of non-tuberculous mycobacterium was around 13%. The most common species were M. avium complex (72%) and M. abscessus (16%).1 Another study suggested that M. abscessus was more common in paediatric patients.2 Clinical signs and symptoms of NTM infections are usually difficult to distinguish from those of chronic respiratory infections that occur during the advanced stages of CF. High-resolution CT often reveals features of parenchymal involvement, as demonstrated in our patient. No guidelines exist for treating NTM infections in the CF population. However, for M. abscessus infection, oral clarithromycin in combination with intravenous amikacin and either cefoxitin or imipenem for 2–4 months has been recommended, with sputum surveillance for at least 12 months after a negative culture result.3 Suppressive maintenance therapy with clarithromycin, intermittent intravenous antibiotics and aerosolised amikacin have all been reported, but not confirmed by controlled studies. Surgical resection may be curative in localised disease. As the life expectancy of patients with CF improves, the prevalence of NTM infections is likely to increase. The American Thoracic Society recommends that all patients with CF who are on macrolide therapy should be screened annually for atypical mycobacteria.3 Atypical mycobacteria should always be borne in mind when treating patients with CF and an unexplained decline in lung function. Computed tomography scan showing diffuse parenchymal involvement, mucus plugging and moderate bronchiectasis in a girl with cystic fibrosis and non-tuberculous mycobacterial lung disease

Abdullah A Yousef · Adam Jaffé

To the Editor: Since colonial times, alcohol has been central to Australia’s political, cultural and social fabric.1 In the past year, concern about alcohol misuse has re-emerged as a dominant feature in the political landscape. We analysed the New South Wales emergency department (ED) data collection, on the NSW Department of Health’s HOIST (Health Outcomes and Information Statistical Toolkit) database, to describe the epidemiology of ED attendances due to acute alcohol problems. Data from 43 hospitals that contributed reasonably complete diagnosis information since 2000 were used. Attendances were selected using codes for alcohol intoxication, alcohol dependence/withdrawal, or drug or alcohol blood test from the ninth and 10th revisions of the International classification of diseases (ICD-9 and ICD-10) or from the Systematized Nomenclature of Medicine — Clinical Terms (SNOMED-CT). Population rates by age, sex and year were calculated. To assess the association between alcohol-related ED presentations and large public social events, time series of 24-hour counts ending at midday were used (because most presentations for acute alcohol problems occur at night).2 Between 2005 and 2008, the rate of ED presentations for acute alcohol problems rose sharply from around 110 to almost 150 per 100 000 population (Box 1). Between 2000 and 2008, the highest rates of ED attendance involved 18–24-year-olds of both sexes, and 25–64-year-old men. The largest increase was among 18–24-year-olds. Notably, in that age group, the rate in women converged with that of men at 228 per 100 000 in 2004 and was then higher until it re-converged in 2008 at around 390 per 100 000. In all years, the rate of presentation in 10–17-year-olds was slightly higher for females than for males (Box 2). Among children aged less than 10 years, the rate was under four per 100 000 in all years. Many peaks in ED attendance coincided with large public gatherings, including New Year’s Eve celebrations and the closing of the 2000 Sydney Olympic Games. In 2007 and 2008 especially, the Sydney Gay and Lesbian Mardi Gras was associated with marked increases (Box 3), which may reflect underlying increases in alcohol use in the younger age groups that might be attracted to this now mainstream event. Because the coverage of the ED data collection was limited, these figures underestimate the true incidence. Nevertheless, most urban and larger rural hospitals were included. We were unable to include the far greater number of ED presentations in which alcohol use was a factor, but not the primary reason for presentation.3 The trends and rates we observed were similar to those found in a recent Victorian study of young people.4 The small decline in overall rate from 2000 to 2002 (Box 1) is consistent with declining per-capita consumption of beer and spirits, while the subsequent increase in young people, which flattened out in 2008, is similar to the trend in consumption of ready-to-drink alcoholic beverages over the same period.5 Studies of the types of beverages used before ED presentation are urgently required to assess whether this is a causal association. Analysis of routine ED databases can provide a timely insight into the social and epidemiological context of high-risk drinking. The rise in alcohol-related presentation among teenagers and young adults bodes poorly for subsequent long-term alcohol use disorders and other risk behaviours and their consequences.6 The correlation between peaks in ED presentations and large-scale social events suggests that the development of cultural norms may have a strong influence on individuals’ behavioural choices. 1 Number and rate of presentations to 43 emergency departments for acute alcohol problems, New South Wales, 2000–2008 Year 2000 2001 2002 2003 2004 2005 2006 2007 2008 Number 6400 6215 6203 6762 6826 7652 9112 10119 10382 Rate per 100 000 population* 98.7 94.5 93.6 101.3 101.7 113.2 133.7 147.1 149.4 * Rates are an underestimate because not all NSW emergency departments are included. 2 Population rate of presentations to 43 emergency departments for acute alcohol problems,* by year, sex and age,† New South Wales, 2000–2008 * Rates are an underestimate because not all NSW emergency departments are included. † Values not shown for people aged < 10 years because all values were below 4/100 000 population. 3 Daily counts* of presentations to 43 emergency departments for acute alcohol problems, New South Wales, 2000–2008 * Counts are aggregated over 24-hour periods, ending at midday.

David J Muscatello · Sarah V Thackway · Daniel A Belshaw · David McGrath

To the Editor: Recycling water from sewage into drinking water was recently discussed in the Journal.1 Although this is technically feasible, we need to be very wary. Such recycling is associated with very high ongoing monetary and energy costs, but, most importantly from a health perspective, is a “very high-risk”2 proposal that reverses 150 years of good public health policy of striving to keep sewage out of our drinking water supplies. When we need to recycle water from highly contaminated sources, it is much safer to do so for industrial purposes using separated pipelines (as is done in Singapore and Brisbane). The most extensive scientific review on this issue concluded that putting it into drinking water should be a “last resort”, that should be adopted only if other measures — including other water sources, nonpotable reuse, and water conservation — have been evaluated and rejected as technically or economically infeasible.3 Sewage contains very high concentrations of pathogens and drugs. Viruses (the most difficult pathogens to remove) can occur in concentrations higher than 106 per litre — orders of magnitude higher than in even the most polluted rivers. The technical and human performance needed to remove viruses safely will have to be proportionately higher than current practice — difficult to achieve, as we already have skills shortages. We would also need to ensure that the system will work all the time. Reverse osmosis (RO) is the most effective way to remove viruses and drugs from sewage, and should remove virtually all viruses and drugs. Surprisingly, few in-use data are available to check this. RO membranes seem to leak. One study found that RO only removed 92% of antibiotics.4 Recent safety reviews, including an Australian review5 (based on the previous study3), showed viruses were still detected post-treatment at three of seven sites on some occasions. The calculated virus removal ranged from 87% to > 99.995%, which equates to a “log reduction” of 1 to 5. However, to produce safe drinking water from sewage, we need a consistent 9.5-log reduction for enteroviruses.2 Even Giardia was not always removed. This less than optimal performance was when the system was not known to be malfunctioning; lowered performance might occur as often as 5 days a year.6 Current surrogate testing (eg, organic carbon) can only detect a membrane leak (or bypass) of at least 1%, which is well short of meeting the 9.5-log reduction we need for virus removal and reasonable safety.2 We need real-time tests to show that there is adequate virus removal, rather than none at all or only becoming aware of a problem after processed but contaminated water is already in our reservoirs.

Peter J Collignon

In reply: We agree that augmentation of drinking water sources with recycled sewage goes against the traditional policy of separating the two, and that many factors including cost and energy use need consideration in securing future water supplies. Our editorial1 was not written to promote potable recycling, which ultimately is a political and societal decision, but rather to point out that the carefully considered Australian guidelines for water recycling2 have been developed to ensure that, if this form of recycling is contemplated, it is done in a manner that safeguards public health. Main messages in the recycling guidelines include the importance of risk assessment for each individual scheme; avoidance of complete reliance on any single technical step (including reverse osmosis) for removal of contaminants, via a “multiple barrier” approach; adequate operational and water quality verification monitoring; and optimising training and skills management within water treatment facilities. Importantly, credits given for “log removal” for each treatment step are based on verifiable on-line performance, not theoretical values.2 These practical messages are also fundamental to the way we manage our conventional drinking water supplies.3 Consequently, discussions about recycling help reinforce the importance of continual assessment of water management, regardless of the source, and help ensure we do not become complacent.

Karin S Leder · Joanne E O’Toole · Martha I Sinclair

To the Editor: The recent withdrawal of faulty faecal occult blood testing (FOBT) kits by the government highlights the flaws in the National Bowel Cancer Screening Program (NBCSP), with 475 000 kits needing to be replaced. In their recent editorial,1 Ee and Olynyk attempted to persuade us that the NBCSP, which has now temporarily suspended the issuing of new invitations to participate, is both rational and appropriate for an affluent country such as Australia. The facts about bowel cancer mortality are not disputed — it is second only to lung cancer, equating to about 12 Australian deaths per day from a potentially preventable cancer. There are only two serious contenders for bowel cancer screening: FOBT and colonoscopy. Annual FOBT has the potential to reduce mortality by 15% (realistic) to 33% (optimistic).2 Colonoscopy is both diagnostic and preventive, with a predicted reduction in mortality of 76% (realistic) to 90% (optimistic).3 Recent United States guidelines advocate colonoscopy at 10-yearly intervals as the test of choice.3 Cost and potential mortality are two major issues raised by proponents of FOBT versus colonoscopy. However, Australian data using all costs, including infrastructure, colonoscopy, surgery, pathology, anaesthesia, chemotherapy and disinfection, have shown that 10-yearly colonoscopy is of equal cost–benefit to annual FOBT.4 A recent publication from Germany highlights some important facts.5 In a study of 269 144 colonoscopies, the completion rate (ie, reaching the caecum) was high, at 97.3%. The perforation rate was low (0.02%), as was the incidence of bleeding (0.16%), though this was predictably greater in those requiring polypectomy (0.8%). There were no deaths attributable to perforation or bleeding. Colonoscopy is therefore a rational option for screening, with the potential for prevention — a feature not shared by FOBT. The NBCSP’s letter of invitation and FOBT kit are sent only to individuals aged 50, 55 and 65 years. It ignores other age groups and gives no educational advice about alternative strategies such as colonoscopy. Ee and Olynyk1 clearly believe that centrally organised government screening programs are to be preferred, and they disapprove of colonoscopy screening “driven by patients”. Recent case series show colonoscopy to be safe and to have a higher completion rate than older series.5 Current initiatives in Australian colonoscopy training programs should improve safety and completion rates further. For those with no active interest in their health, centralised, directive programs are likely to be the most effective. For the informed, however, discussion about lifestyle changes, screening programs and healthy dietary alternatives should be their right.

Terry D Bolin · Melvyn G Korman · Alistair E Cowen

To the Editor: Australia’s world-leading government-funded National Human Papillomavirus (HPV) Vaccination Program for women aged 12–26 years is made up of two components: an ongoing school-based program and a time-limited catch-up program delivered through schools, general practices and community vaccination services. The catch-up program started in April 2007 and was due to finish by July 2009, but has been extended to 31 December 2009 to allow women to complete the three-dose schedule. Assessing the coverage achieved by the National HPV Vaccination Program will be an important measure of the Program’s success, particularly in terms of ensuring equity in vaccine uptake — so that the current gap in cervical cancer incidence and mortality between Indigenous and non-Indigenous women is reduced, not widened.1 Vaccination coverage data are also needed to monitor vaccine effectiveness in preventing cervical lesions and cancer. Accordingly, an integral part of the Program was the establishment, enabled by legislation passed in August 2007, of Australia’s first national adult vaccine register — the National HPV Vaccination Program Register. The Register began collecting data in mid 2008 and is currently uploading notifications of the 5 million doses of HPV vaccine distributed in Australia to date. Initial coverage estimates from the Register will be published by the end of the year, with all notifications from the catch-up program due to be submitted to the Register by March 2010. General practitioner incentive payments of $6 per notification will be available until that time. Interim coverage data provided by various jurisdictions are encouraging; school-based program data for 2007 from New South Wales and Victoria estimate one-dose coverage of more than 80% and three-dose coverage of approximately 70%.2 Unfortunately, there are no routine systems in place to provisionally estimate coverage in women vaccinated outside of schools. In a small population-based telephone survey that was conducted by the Cancer Council Victoria 3 months after the Program commenced, 35 of 90 women aged 18–26 years (39%) had received HPV vaccine. Australian women are taking advantage of Australia’s most expensive vaccination program to date. We encourage vaccination providers to notify the Register3 of doses administered to ensure that this facet of Australian women’s health can be followed into the future. Although we anticipate complete notification of vaccinations given at schools, the accuracy and completeness of total coverage data will depend on GPs notifying the Register.

Julia M L Brotherton · Robyn M Mullins

To the Editor: Over a third of women seeking a termination of pregnancy (TOP) in Melbourne are aged 30 years or over.1 Between 1996 and 2006, there was a 29% increase in the number of women aged 30–50 years having a TOP.2 Possible reasons for this trend are not immediately apparent. We audited the files of 50 consecutive women aged 35 years and over attending a private termination service in metropolitan Melbourne in February 2007 to determine reasons for deciding on a TOP and the women’s prior and intended contraceptive use. Of the 50 women, 38 were working in paid employment, 28 had private health insurance, 39 had at least one child, 22 had had at least one previous TOP, and 43 were in an ongoing relationship. Sixteen separate reasons for TOP were elicited (Box), with nearly three-quarters of the women citing more than three reasons for terminating their pregnancy. Over a third of the women cited financial pressures, a focus on career or studies, having dependent children, or emotional unpreparedness for children as reasons for having a TOP. Contraceptive methods used by the 29 women who indicated their prior contraceptive practice were as follows: none (9), condoms (8), natural family planning (NFP) (4), the combined oral contraceptive pill (COCP) (4), withdrawal (3), and the mini pill (1). After the TOP, contraceptive methods chosen were the COCP (11), vasectomy (10), an intrauterine device (10), condoms (8), the mini pill (5), an etonogestrel implant (4) and NFP (1). Although ours was a small retrospective audit, the contraceptive findings and reasons given for TOP in our study were similar to those of other studies.1-4 However, some of the reasons given for TOP in this age group have not previously been described — for example, having ageing parents to care for, recent migration to Australia, and ambivalence towards parenting. Furthermore, although recent Australian studies have reported a high level of contraceptive use,2,5 women in our study often relied on less effective forms of contraception or no contraception at all. Further qualitative research is needed in women of this age group to explore their understanding of fertility and pregnancy risk, barriers to effective contraceptive use, and additional supports and interventions that could prevent unplanned pregnancy in these women. Reasons for termination of pregnancy among 50 women aged ≥ 35 years Reason Number citing reason Already have dependent children 17 Focus on career or studies 17 Emotionally unprepared for a child 16 Financial pressures 16 Completed family 15 Relationship factors 14 Too old to raise a child 10 Partner factors, including partner not wanting children 9 Physical or psychological health issues 8 Concerns about congenital anomalies 7 Does not want single parenthood 6 Bad timing (recent job change, move home, move to Australia) 4 Uncertain of wanting children or does not want children 4 Exposure to medications or agents that might harm fetus 1 Pregnancy from sexual assault 1 Other factors (other life plans, uncertain paternity, poor social supports, aged dependent parents) 9

Wendy Lee · Danielle Mazza

To the Editor: We agree with Stockigt that clinical accountability is needed in the production of consumer medicines information (CMI).1 However, providing CMI is a great deal more complex. The ways in which consumers access and absorb medical information are still largely unknown, and the most important issue is potentially that consumers are not receiving CMI. The benefits of involving consumers in shaping health research and medical policy are widely acknowledged.2,3 We recently completed a study funded by the National Health and Medical Research Council (NHMRC) on improving medication safety and chronic disease outcomes in people aged over 65 years, which was accepted for presentation at the national General Practice and Primary Health Care Research Conference in Melbourne, July 2009. Three community forums co-facilitated by the Health Consumers’ Council of Western Australia raised key issues around the safe use of medicines, and an expert panel of consumers aged over 65 years was convened to guide the study. The safe use of medicines was then qualitatively explored in a series of focus groups and individual interviews. Our findings add to those of Vitry and colleagues,4 and suggest that campaigns urging consumers to request CMI may fall short of what is required to make a difference. We found that most study participants did not know they could ask for a CMI printout at the pharmacy. They noted that if the pharmacist was busy, they would not ask for advice or CMI, even if they were uncertain of dosages or potential side effects or interactions. Given that medication side effects and interactions were the greatest concerns for this age group, it is troubling that CMI is not getting to those who need it. In addition, it was noted that participants were not selective in accessing alternative web-based information about medicines, believing it to be reliable because it is “written by medical professionals”. A further issue raised by participants was a perception of undue influence of pharmaceutical companies on the prescribing choices of general practitioners, leading to mistrust of medicines information provided by doctors. Clearly, there is still more to be done to ensure consumers receive the right information at the right time about their medicines.

Caroline E Bulsara · Anne McKenzie

To the Editor: We share Millar’s concerns about the conflicts of interest that influence the genesis and adoption of clinical guidelines1 specifically, and the lack of independent assessment regarding information provided by the pharmaceutical industry generally. Iain Chalmers puts it succinctly: I do not blame industry for trying to get away with anything that is normally considered to be its primary purpose, which is to make profits and look after its shareholders’ interests. It is our profession that has colluded in all of this and been prepared to go along with it — we are the people to blame because we need not have stood for it.2 We believe the reasons behind this acquiescence are complex, but worthy of discussion. A strong and viable pharmaceutical industry is essential for clinical improvement. Similarly, clinical involvement in industry research is necessary. We would not debate either of these statements, but we are concerned about the failure of our profession to stand back and exercise careful scrutiny of data. Classic examples are thalidomide in the 1960s and, more recently, the cyclooxygenase-2 (COX-2) inhibitors, but many less dramatic examples can be found, such as gatifloxacin or rosiglitazone. This failure on our part harms both patients and the standing of our profession. A recent article in this Journal suggested this failure of physician leadership may in part be due to the comfortable position we cultivate with industry,3 relationships that go beyond the business transaction of providing independent medical advice for a consulting fee. Further, the role of “key opinion leaders”, cultivated by industry, is reinforced by criteria for hospital accreditation and university promotion, leading to disproportionate value being placed on service to company boards (which is often paid and of modest time commitment) compared with service on hospital, state and national regulatory and quality committees (which is usually time-consuming and unpaid). The presupposition in this discrepancy is that physicians on the company circuit are better physicians than those who are not. We should all support the recommendations of Millar,1 Olver and Haines,3 and Van Der Weyden,4 including those for true independence and transparency of guideline development and dissemination, strengthening ethical administrative structures and placing appropriate value on public service. Upskilling of clinicians in epidemiology and critical analysis is thus urgently needed so the incremental benefit and costs of new therapies can be objectively examined.

Jennifer H Martin · Christopher Beer · Raymond G Morris · Matthew P Doogue

To the Editor: Articles by Olver and Haines1,2 have catalysed robust discussion about the relationship between the pharmaceutical and device industries and the medical profession.3 These authors advocate changes in the direction of clinical cancer research and in health policy.2 In an era in which research into medicines is dominated by industry, they argue for greater scrutiny of data in a resource-constrained environment, and for fundamental changes in the collection, interpretation and ownership of data. We find their arguments sound and equally applicable to other areas of medicines research and health policy. Their primary recommendation is for “. . . a system to follow up and evaluate the outcomes of all treatments . . .” That is, that we exercise our duty to patients by monitoring and analysing existing clinical data to inform health care policy. There is a great deal of valuable clinical data collected that are not readily accessible because of ownership or privacy issues. For example, much business involving public health dollars is labelled “commercial in confidence”, and laboratory data held in many pathology databases are not accessible at all. The likely benefits to patients and society of transparency and data linkage in health care are greater than possible benefits to individuals of secrecy and privacy. Quality use of medicines (QUM) is one of the central objectives of Australia’s national medicines policy. QUM means selecting management options wisely; choosing suitable medicines if a medicine is considered necessary; and using medicines safely and effectively.4 Olver and Haines also identify issues relating to quality use of research. Quality use of research might include: supporting research into monitoring clinical outcomes related to drug use; supporting research into better use of existing drugs; and supporting truly independent guideline development. There continue to be advances. For example, registration of trials in public databases, such as the Australian New Zealand Clinical Trials Registry, should reduce publication bias.5 However, the decline of independent public sector clinical drug research and the marketing-based design of phase III and, increasingly, phase II industry-funded studies contribute additional bias to the available information. Olver and Haines’ arguments apply to all therapeutics, and particularly to all drug therapies. We strongly support their proposals for health data linkage and for quality use of research. These fit within existing health policy, and our continued failure to make full use of clinical data is an ethically compelling reason for improved political and clinical governance.

Matthew P Doogue · Kathleen M Knights

To the Editor: The expert working party that developed the Australian Medical Council (AMC) draft code of professional conduct referred to by Komesaroff and Kerridge1 was chaired by Joanna Flynn, past President of the Victorian Medical Practitioners Board (MPB [Vic]). Herein lies the crunch. The AMC is surely meant to be an independent and objective body — yet if it is aligned with the MPB (Vic), how can this be the case? Komesaroff and Kerridge state that the appendices to the AMC’s draft code “quote extensively (without attribution) the conclusions of guidelines developed by the Royal Australasian College of Physicians” and that “in the AMC’s version, the evidence, context and argumentation are omitted and the recommendations are presented as legally binding”.1 If this is the case, there is cause to question the integrity of the drafters of the code, to fear the code’s implications, and to request “that the whole process that gave rise to it be rigorously reconsidered”.1 Plagiarism cannot be condoned. To attribute honestly and give credit where credit is due is central to ethical practice, scientific discovery, education, accountability and learning. Similarly, context matters. In my opinion, integrity, the basis of ethics and morality, is measured by the extent to which context is valued and conceded. Ethical conduct demands both honesty and integrity. Doctors and the public, and government surely, place their trust in the AMC to objectively evaluate governing practices, laws and regulations, such as the Health Professions Registration Act 2005 (Vic) (“the HPR Act”), under which the MPB (Vic) operates, as well as professional conduct. Yet the authors of the AMC draft code fail to address the issue of the accountability of regulatory bodies and the fact that the HPR Act contains no benchmark for excellence: because context is omitted from the Act, “unprofessional conduct” cannot be defined and becomes relative. This leaves it open for any third party, including members of the regulatory authority itself, to abuse doctors and patients by being dismissive of the patient’s view (and thus, context), while claiming to protect patients and guide doctors. By contrast, the Medical Treatment Act 1988 (Vic), which is not mentioned in the AMC draft code, provides a benchmark for excellence in clinical practice with reference to both doctors and patients. This Act specifies (a) that the wishes of the patient to refuse treatment be respected, and (b) that medical practitioners who act in good faith in accordance with the patient’s expressed wishes be protected from any civil or criminal liability or disciplinary action by the regulatory board.2 As doctors, we are the naturally appointed advocates of our patients’ health preferences and wellbeing. Ensuring that choices are made for the patient’s benefit requires honesty and integrity at all levels of government.1,3,4 When a failure occurs in the system, it is imperative to have avenues of awareness, transparency, protection and evaluation available through public action and professional debate.1,3,5

John B Myers

In reply: The debate about the proposed national code of conduct (“the Code”) has raised a number of important issues, including those highlighted by Myers. The original draft aroused serious concern in the community about the potential role of a centralised bureaucracy with the power to enforce a set of precepts derived from a narrow, largely discredited, philosophical perspective. Although the revised draft now circulated for public comment is admittedly less objectionable than its predecessor, significant concerns remain relating to both its form and its content. The main issues are still the purpose and role of the Code and the confusion between ethical and legal discourses on which it is based. In a multicultural society in which pluralism and diversity are themselves regarded as inherently valuable, the very concept of a unitary set of criteria that define good practice is questionable. In this setting, the proper roles of codes of conduct and of ethics are not to enforce particular kinds of outcomes, but rather to inform and enrich practice. If the Code were devised as an educational process to stimulate clinicians to reflect critically on their existing practices and underlying values, it would be much more likely to change behaviour and increase community wellbeing.

Paul A Komesaroff · Ian H Kerridge

To the Editor: The relationship between population, climate warming and environmental impact has been little discussed in the Australian medical media and often ignored in the wider Australian media. All doctors should have a good working knowledge of the science of climate change and its correlation with increased human activity. Six billion humans (circa 2000 ad) have a greater environmental impact than one billion humans (circa 1800 ad), and this increase correlates with deterioration in nature’s “free goods”, such as clean air and water. Globally, demand for food is outstripping supply, resulting in malnutrition and starvation for the world’s poorest. Nationally, changes in the Australian climate have the potential for increased prevalence of tropical diseases, and extreme weather events can cause damage to infrastructure (including health facilities), social dislocation, injury and death. Guillebaud and Hayes argue that doctors must lead the discussion on population growth and climate change.1 They point out that the global population increase of 1.5 million each week equates to a huge new city ... which destroys wildlife habitats and augments world fossil fuel consumption. Every person born adds to greenhouse gas emissions ...1 Those who insist on the right to a large family must also consider the wider social implications of population growth,2 although there is little to be gained by recriminations against those who have already formed large families. We should take the perspective of retired physician Bryan Furnass: address the problems — population, pollution and poverty — with the solutions — ecology, education and ethics.3 Those doctors who understand the methods used by the tobacco industry to subvert the community’s appreciation of the risks of smoking will also understand that similar tactics can and are being employed by those with vested interests in high carbon-emitting industries. Their arguments are based on a belief that technology can solve all problems, while hiding the relationship between increased total consumption, profit and population growth. We need to understand and lead the community’s discussions on global overpopulation and health reduction. Australian doctors are lagging behind in this. British doctors are already publishing on this topic,4 and the Australian Parliament has commenced discussion on the need for a population policy.5 It is time for Australian doctors to read, discuss, research, write and, following the lead of Walters,6 publish constructively on population growth and its impact.

Robin I W Collin

To the Editor: On my way to Canberra for the Charles Darwin exhibition at the National Museum of Australia, I diverted to Pambula, on the far south coast of New South Wales, for two reasons. Pambula is part of the Australian connection with Darwin through Syms Covington, who, at the age of 15, sailed as a cabin boy on the Beagle in 1831. Darwin soon came to rely on Covington to collect specimens, excavate fossils and act as his personal assistant. During the Beagle’s brief visit to Sydney, Covington was impressed by the colony. In 1840, after a period of employment with Darwin in England, he returned to Australia and eventually became a wealthy man. At first he lived in Sydney, but by 1854 had moved to Pambula, where he became postmaster. His entrepreneurial activities included buying large tracts of land around the Pambula River and the little township of Pambula. On a large block, he built a house of solid sandstone bricks with cedar woodwork throughout — “Covington’s Retreat”. Covington continued to correspond with Darwin and, at the latter’s request, collected specimens for him. He died in 1861. The house, at 28 Quondola Street, still stands and has been listed by the National Trust of Australia (NSW) in Heritage Council File HC32549. After being used for various purposes, including as an inn and as a police station, it became the residence of the local doctor, probably around the start of the 20th century — hence my second reason for visiting Pambula. The subsequent careers of some of the Pambula general practitioners, all of whom lived in the house, are of considerable interest. All came to Pambula from outside the area. Grace Cuthbert (later Cuthbert Browne), MBE, left Pambula in 1929. She was Director of the Division of Maternal and Baby Welfare of the NSW Department of Public Health (1937–1965) and, among many other positions, President of the Australian Federation of Medical Women. Naomi Wing, CBE, and her husband Lindon practised in Pambula from 1929 to 1936. She was an early advocate of rehabilitation medicine as a medical discipline and became President of the Australian Association of Physical and Rehabilitation Medicine. The Naomi Wing Rehabilitation Centre in Zetland, Sydney, was named in her honour. Her husband, Lindon Worlledge Wing, KStJ, was an early practitioner of occupational medicine in Sydney. Their son, Emeritus Professor Lindon Michael Harper Wing, was Dean of the Medical School at Flinders University, Adelaide, from 1998 to 2007. From 1936 to 1945, the house was owned by Keith Jones, who went to World War II from Pambula and whose name is on the town’s war memorial. After the war, he became a surgeon and, over the years, undertook a wide range of community activities. He was President of the Australian Medical Association (1973–1976), Chairman of the Australasian Medical Publishing Company Limited (1976–1982) and, for a time, Acting Editor of the Medical Journal of Australia. He was knighted in 1980. Covington’s Retreat is now a Thai restaurant called “Covingtons Thai”.

George D Repin

To the Editor: We both are ear, nose and throat (ENT) specialists at a tertiary university hospital and cover 1–2 nights of emergency calls each month. Over 8 months in 2008, we witnessed four emergency patients (aged 25–39 years; three men, one woman) who had sore throat, mild fever and pain on swallowing, without any respiratory distress symptoms. One patient presented with “hot potato voice”. All had had a palatine tonsillectomy in childhood. On examination, the oral pharynx appeared normal to mildly hyperaemic, without any suppuration. To exclude potentially fatal epiglottitis, all patients underwent transnasal flexible laryngoscopy, which revealed swollen lingual tonsils covered with fibrinous exudate typical of streptococcal infection. Distal structures, including the epiglottis and endolarynx, were normal. Acute lingual tonsillitis was diagnosed, and the patients quickly responded to penicillin therapy. Some degree of infection of the lingual tonsils probably occurs when the pharynx is otherwise infected, but is usually left undiagnosed because it is not easily visible without laryngoscopy.1 Although none of our patients had any life-threatening symptoms, this condition could potentially cause upper airway compromise, and the course would certainly be more arduous without antibiotics. The flexibility of our health care system in Croatia allows for some emergency patients’ to refer themselves to the relevant specialty services. If these patients had presented to general practice rather than to our department, where we performed transnasal laryngoscopy, this diagnosis would have probably gone unnoticed, and antibiotic therapy would not have been prescribed. Thus, is acute lingual tonsillitis a neglected cause of severe sore throat? A search of the current literature and ENT textbooks did not reveal many reports of this disease.2,3 Even if our observations referred to rare cases, considering our hospital catchment population for ENT emergencies of more than 300 000, they still outnumbered all cases of epiglottitis treated at our emergency service during the same period. Therefore, it is our opinion that acute lingual tonsillitis should be at least kept in mind as a condition that can cause severe sore throat that is oropharyngoscopically silent or mimics simple viral infection, but is effectively and readily treated with antibiotics.4 Because the base of the tongue cannot be visualised by routine intraoral examination, confirmation of the diagnosis must be made by an ENT specialist who will perform laryngoscopy.

Sasa Janjanin · Drago Prgomet

To the Editor: We read with interest the work presented by Markovic and Natoli, highlighting the importance of recognising the nutrient density of foods in managing overweight and obese patients.1 We present data to support their observation that it should not be assumed that a patient who is overweight or obese has a nutritionally adequate diet. Our data were obtained as part of the Geelong Osteoporosis Study from an age-stratified sample of men randomly selected from electoral rolls for the Barwon Statistical Division in Victoria. Dietary intake was estimated using a food frequency questionnaire developed by the Cancer Council Victoria.2 Basal metabolic rate (BMR) was estimated from the Schofield equations, based on age and weight. Data were excluded if the ratio of energy intake (EI) (from food and alcohol combined) to BMR was < 0.9. The sample comprised 1175 men aged 20–93 years (median age, 56 years [interquartile range, 39–73 years]; mean weight, 81 kg [SD, 14 kg]; mean height, 1.75 m [SD, 0.07 m]). Participants were grouped by body mass index (BMI) into three categories: normal weight (BMI < 25 kg/m2), overweight (BMI 25.0–29.9 kg/m2) and obese (BMI ≥ 30 kg/m2). Estimates of physical activity were derived from self-report. Written, informed consent was obtained from participants, and the study was approved by the Barwon Health Human Research Ethics Committee. We investigated the breakdown of macronutrients, vitamins and minerals listed in the “virtual” case report presented by Markovic and Natoli1 and expressed intakes as a percentage of recommended dietary intake (RDI).3,4 Despite adequate EI, the diets of men in all BMI categories were low in zinc, calcium, folate and fibre (Box). We acknowledge that there are limitations posed by self-reported dietary intakes and physical activity levels. The EI–BMR ratio decreased with increasing BMI (median [interquartile range], 1.4 (1.2–1.7), 1.3 (1.1–1.6) and 1.2 (1.0–1.5) for normal weight, overweight and obese subjects, respectively), suggesting that under-reporting may have been more common with increasing BMI. We also acknowledge that RDIs are not thresholds for dietary deficiencies. Within these constraints, however, these data suggest that where there are nutritional shortcomings in diets, they are not limited to men of normal weight-for-height, but are also apparent among those who are overweight and obese. These shortcomings suggest that nutrient-dense foods, such as whole grains and vegetables (particularly leafy green vegetables) are underconsumed, while processed foods with high saturated fat and salt content are consumed excessively. These observations underscore the importance of recognising the nutrient density of foods so that nutrition is not compromised when EI is restricted. Nutritional intake expressed as a percentage of recommended dietary intake (RDI) in a cohort of 1175 men,* by weight category† Nutrient RDI3 Normal weight (n = 471)‡ Overweight (n = 530)‡ Obese (n = 174)‡ Energy (kJ) § 92% (78%–111%) 97% (83%–119%) 105% (88%–124%) Protein (g) 64 (20–70 y); 81 (> 70 y) 139% (109%–181%) 143% (115%–185%) 157% (124%–195%) Total fat (g) 70* 124% (97%–158%) 123% (97%–153%) 127% (102%–173%) Saturated fat (g) 24* 146% (112%–190%) 145% (109%–188%) 154% (115%–206%) Carbohydrate (g) 310* 77% (64%–94%) 78% (65%–92%) 77% (65%–90%) Sugar (g) 90* 117% (90%–142%) 115% (88%–148%) 106% (84%–131%) Fibre (g) 30¶ 78% (60%–100%) 80% (61%–99%) 80% (64%–98%) Iron (mg) 8 173% (136%–225%) 180% (148%–223%) 185% (151%–229%) Zinc (mg) 14 88% (69%–110%) 92% (74%–113%) 93% (79%–120%) Calcium (mg) 1000 (20–70 y); 1300 (> 70 y) 87% (66%–117%) 89% (70%–116%) 90% (68%–109%) Folate (μg) 400 78% (62%–99%) 81% (64%–99%) 82% (67%–102%) Vitamin C (mg) 45 279% (194%–402%) 283% (204%–409%) 294% (213%–434%) Vitamin A (μg) 900 100% (80%–131%) 104% (82%–126%) 104% (82%–127%) Sodium (mg) 460–920¶ 306% (247%–399%) to 611% (494%–799%) 314% (259%–382%) to 628% (518%–764%) 345% (258%–412%) to 690% (515%–824%) BMI = body mass index. y = years. * As no National Health and Medical Research Council (NHMRC) RDIs exist for total fat, saturated fat, carbohydrate and sugar, we used Food Standards Australia New Zealand RDI values for these nutrients.4 † Normal weight, BMI < 25 kg/m2; overweight, BMI 25.0–29.9 kg/m2; obese, BMI ≥ 30 kg/m2. ‡ Data are presented as median (interquartile range). § RDI for energy was based on age and height and a physical activity factor derived from self-report. ¶ Adequate intake.

Julie A Pasco · Margaret J Henry · Mark A Kotowicz · Geoffrey C Nicholson

To the Editor: Markovic and Natoli draw attention to the frequent presence of nutritional deficiencies in obesity.1 While the authors detail various nutrient deficiencies that may arise from a nutrient-poor diet, they do not discuss the possibility of vitamin D deficiency. Normally the main source of vitamin D is that synthesised in skin exposed to ultraviolet B radiation. A nutrient-rich or nutrient-poor diet alone is unlikely to provide adequate vitamin D unless foods are supplemented with vitamin D. Vitamin D deficiency in obese people is prevalent, and Holick has described an inverse relationship between body mass index and 25-hydroxyvitamin D levels, with sequestration of vitamin D in body fat reducing its availability.2 Vitamin D deficiency is associated with various conditions for which obesity is a risk factor, including cancer, depression, altered glucose metabolism and cardiovascular disease.2 A prospective study would be required to determine whether vitamin D supplementation is able to modify some of these associations. Increasing vitamin D levels are associated with improved muscle strength,2 and thus vitamin D supplements may be of benefit in obese patients with reduced vitamin D levels. Furthermore, combined vitamin D and calcium supplementation may have a small beneficial role in preventing type 2 diabetes.3 Pending more evidence, it would be prudent to consider measuring 25-hydroxyvitamin D levels in obese people and correcting any deficiency. In view of the large amount of adipose tissue in obese people, it is likely that they would require higher than normal doses to achieve repletion of their vitamin D stores.

Barbara Depczynski

To the Editor: We concur wholeheartedly with Gill and colleagues1 in support of recognising obesity as a public health issue, and we dispute claims that the current problem of obesity is being exaggerated. Gill and colleagues point out that obesity trends have climbed over decades, and state that 6%–8% of Australian school children are affected.1 While this is a substantial burden of over a quarter of a million children, we also consider that restricting definitions of obese to arbitrary cutoff points may underestimate the problem, given that the entire distribution of childhood weight is increasing, not just the extreme group classified as obese. Adiposity is related to cardiovascular outcomes such as myocardial infarction and stroke in a (curvi)linear fashion. Defining obesity by arbitrary cutoff points is vulnerable to differences between sexes, ethnicity and age, and limits our understanding of obesity-related diseases. It is well known that cardiovascular risk factors cluster, particularly the adiposity-driven components of the so-called metabolic syndrome. In the Western Australian Pregnancy Cohort (Raine) Study, we have used cluster analysis to identify a group of children at risk of future cardiovascular disease with features of the metabolic syndrome.2 The differences in characteristics are shown in the Box. The “high risk” and “low risk” cluster groups differ widely in terms of not only body mass index, the most widely used measure of obesity, but also waist circumference (a measure of central adiposity), insulin resistance, blood pressure, and levels of triglycerides, high-density lipoprotein cholesterol, total cholesterol (data not shown) and low-density lipoprotein cholesterol (data not shown). Not only the conventionally used 95% confidence intervals, but also the 99% confidence intervals do not overlap for any of these intermediate cardiovascular risk factors. We found that 29% of children were in the high-risk cluster at the age of 14 years2 and a similar analysis suggested that even at age 8 years, 25% of children were at increased risk of future obesity, cardiovascular disease and diabetes.3 C-reactive protein (CRP) level is known to be associated with future cardiovascular diseases in adults,4 and with an adverse metabolic profile in children.5 The “high risk” children had significantly higher CRP levels at the age of 14 years than their low-risk counterparts. Certainly, the magnitude of this problem, affecting up to a third of our youth, needs to be addressed by government and health-planning bodies. We suggest our approach of cluster analysis will help identify earlier those children at substantially increased risk of cardiovascular and other adiposity-related disorders in Australia. Features of the cluster groups with respect to components of the metabolic syndrome, showing 99% CIs* BMI = body mass index. HOMA = homeostatic model assessment (for quantifying insulin resistance). SBP = systolic blood pressure. HDL = high-density lipoprotein cholesterol. * From Huang et al.2 Reprinted with permission from the American Diabetes Association.

Rae-Chi Huang · Fiona J Stanley · Lawrence J Beilin

To the Editor: There is a substantial volume of evidence from a range of national and state-based surveys illustrating increases in the rates of obesity and overweight among Australian children over the past two decades,1 concurring with trends observed in most developed countries.2 The recent article by Gill and colleagues highlighted questions that have been raised publicly regarding the extent and impact of levels of obesity and overweight among Australian children, including whether trends have been exaggerated.1 To examine these issues using the latest data available, we present data from the three most recent national surveys in which weight and height of Australian children were measured: the Australian Health and Fitness Survey (1985),3 the National Nutrition Survey (1995),4 and the Australian National Children’s Nutrition and Physical Activity Survey (2007).5 We examined overweight and obesity levels among young Australians from comparable age groups at three time points over more than 20 years, using the same internationally accepted definitions of childhood overweight and obesity. For 1985 and 1995 data, we used the figures reported by Magarey et al in 2001,6 which compared results from the 1985 and 1995 surveys using new standard international definitions to classify overweight and obesity among Australian children and adolescents.7 We calculated body mass index for the 2007 Australian National Children’s Nutrition and Physical Activity Survey using the raw data file obtained through the Australian Social Science Data Archive,8 categorising children as overweight or obese based on the same international definitions used by Magarey et al.6 We based our calculations on the age group common to each of the three surveys: 7–15-year-olds. As shown in the Box, the prevalence of overweight and obesity in boys aged 7–15 years has risen from 11.0% (95% CI, 10.99%–11.01%) in 1985 to 20.0% (95% CI, 19.97%–20.03%) in 1995 and 23.7% (95% CI, 23.68%–23.72%) in 2007. In 7–15-year-old girls, the prevalence of overweight and obesity has increased from 12.2% (95% CI, 12.19%–12.21%) in 1985 to 21.5% (95% CI, 21.47%–21.53%) in 1995 and 25.8% (95% CI, 25.78%–25.82%) in 2007. While data from additional time points are required to map national trends more comprehensively, our analysis clearly indicates an upward trend in overweight and obesity levels in both boys and girls aged 7–15 years between 1985, 1995 and 2007. This trend is cause for alarm, given the widely recognised body of evidence on the significant short-term and long-term consequences of childhood obesity.9 Prevalence of overweight and obesity in Australian children aged 7–15 years, 1985–2007 * Data weighted for age, sex and region with the weighting variable in the raw data file obtained from the Australian Social Science Data Archive.8

Lyn M Roberts · Tessa R Letcher · Alexandra A Gason · Tim Lobstein

To the Editor: Davis and colleagues stated that the Framingham and United Kingdom Prospective Diabetes Study (UKPDS) cardiovascular risk equations are not suitable for predicting risk in an Australian population with type 2 diabetes.1 If confirmed, this would be extremely disappointing. However, before accepting this conclusion the following important considerations should be noted. Davis noted that the Fremantle Diabetes Study (FDS) patient group differed significantly from the UKPDS baseline group (eg, 38% of the FDS patients were aged outside the validated age range of the risk engine [25–65 years] and were assessed by non-validated extrapolation). Similarly, it cannot be assumed that the FDS group is representative of patients in general practice and hospital diabetes clinics around Australia. Moreover, it would be interesting to know how well the engine performs in FDS patients in the age group in which it was validated (ie, patients diagnosed with diabetes at age 25–65 years). It is likely that the low rate of cardiovascular events in the FDS (4.8% with at least one myocardial infarction, and 2.9% with at least one stroke)1 affects the accuracy of the results obtained with the UKPDS risk engine. The Framingham risk score has already been found to vary considerably in accuracy between populations, with predicted-to-observed ratios ranging from underprediction of 0.43 to overprediction of 2.87.2 Further, the UKPDS risk engine recently overestimated the risk of cardiovascular disease events in a UK general practice population.3 In purely pragmatic terms, most patients with type 2 diabetes aged over 50 years are at “high risk” for cardiovascular events (cardiovascular risk of more than 20% over 10 years),4 and the UKPDS risk engine is unlikely to influence prescribing practice significantly. However, we have found the engine to be a useful educational tool for explaining risk to patients. Even if the UKPDS risk engine is not optimally calibrated, the FDS analysis revealed that the coronary heart disease risk equation had modest discrimination (area under the receiver operating characteristic curve [AUC], 0.68), and the stroke risk equation had good discrimination (AUC ≥ 0.86),1 identifying those at highest risk. We believe that, rather than being irrelevant in Australians, the UKPDS risk engine continues to identify those at highest risk for cardiovascular events, operates well within its validated age group, and provides a motivational tool for encouraging changes in patient behaviour. Until a large dataset is pooled from various Australian studies, we believe the UKPDS risk engine should not be discarded.

Roland W McCallum · John R Burgess · Timothy M Greenaway

In reply: We thank McCallum and colleagues for their comments. In relation to their specific points: The Fremantle Diabetes Study (FDS) cohort is representative and drawn from a typical Australian urban centre.1 The 488 cardiovascular disease-free FDS participants with type 2 diabetes who were aged 25–65 years at both diagnosis and study entry had 22 coronary heart disease (CHD) events compared with 72 predicted, with a similar area under the receiver operating characteristic curve (AUC) to that for all 791 patients who were included in the analysis2 (0.66 v 0.68). Calibration indicated significant discrepancies between predicted and actual outcomes (P ≤ 0.02), and positive predictive values were low (≤ 3.5%). Therefore, restricting our patient sample to a “UKPDS” cohort did not alter our conclusions. We agree that the low observed CHD event rate in the FDS compared with that predicted by the UKPDS risk engine undermines its validity in Australians with type 2 diabetes. There was a similarly low CHD event rate in the FIELD study, which included many Australasians.3 Contemporary diabetes care clearly differs from that during the Framingham Study and UKPDS. Although the study cited by McCallum and colleagues, in a UK general practice population, is not strictly comparable to our study, it also found that the UKPDS cardiovascular disease risk engine performed only moderately (AUC, 0.72).4 Accurate risk prediction should be a basis for cost-effective care. We have developed an FDS risk calculator which should improve clinical management for Australians with diabetes.5

Wendy A Davis · Stephen Colagiuri · Timothy M E Davis

To the Editor: The federal government is to be applauded for its decision to re-introduce the “alcopops” tax Bill to Parliament and to try to retain the $300 million raised so far for expenditure on services, programs and research to reduce alcohol-related harm in Australia. The alcopops tax was paid by consumers in the form of higher retail prices, which will fall dramatically if the government again fails to pass legislation to retain the tax. If it transpires that the government cannot retain the revenue already raised, it should be given to an independent public health body (such as the National Health and Medical Research Council [NHMRC]) and not to DrinkWise via distillers and distributors, as has been suggested.1 DrinkWise is a “putatively independent body that was originally funded by the alcohol industry”;2 six of the 11 current members of its board are senior alcohol industry figures. The alcohol industry profits from drinking that contributes significant harm to individuals and communities,2 and it can be relied upon to oppose policies that are known to reduce alcohol consumption across the population.3,4 DrinkWise and similar industry-backed organisations around the world promote industry-friendly programs that do not have an evidence base or are ineffective (such as education campaigns or tepid television advertising),5 while lobbying against the adoption of effective evidence-based interventions, such as higher taxes on alcohol, as these would affect profits.2-4 The Chief Executive of DrinkWise, Chris Watters, recently revealed the organisation’s position on the alcopops tax, reportedly asserting that it did not recommend “fiddling with alcohol tax” because it was “old thinking” and that “the facts just don’t stand up”, and noting that DrinkWise funds many educational programs across the country.6 There is a clear consensus among public health experts worldwide that increasing the price of alcoholic beverages is one of the most powerful and cost-effective strategies that governments have at their disposal to reduce unhealthy alcohol use.7-10 Other effective strategies include drink-driving legislation, random breath testing, increasing the minimum legal age for drinking or purchasing alcohol, restrictions on trading hours and numbers of licensed premises, and better enforcement of existing liquor laws. In contrast, comprehensive reviews of the evidence show that, by themselves, alcohol education programs are ineffective.11,12 Alcohol industry-sponsored agencies have adopted similar public relations strategies to those used by the tobacco industry.3 These strategies distract attention from their concurrent lobbying against the adoption of policies that would actually make a difference. The laudable policy action taken thus far by the government in its attempt to implement the alcopops tax would be enhanced by supporting an independent body, such as the NHMRC, that has transparent funding strategies and criteria, based on an independent peer-review system, to distribute funding for alcohol-related research. We, along with the more than 50 other scientists and health experts listed at <http://www.webcitation.org/5gbwQWf9J> who endorse and are signatories to this letter,13 will not seek or accept funding from DrinkWise. We call on other researchers and community agencies to consider their positions.

Peter G Miller · Kypros Kypri · Tanya N Chikritzhs · Steven J Skov · George Rubin

In reply: I write in response to the letter from Miller and colleagues, recently published online.1 Their letter is an attempt to influence non-government senators as the Australian Government reintroduces the Bill to increase the tax on some alcoholic beverages. There must have been a better way to do this than by besmirching the good work of DrinkWise and its directors. DrinkWise Australia is not an industry-dominated body. It has a balanced board of six members from the alcohol industry and six distinguished community members. Miller and colleagues should know that, in criticising DrinkWise, they also attack the reputations of board members Professor Ross Kalucy, Chair of Psychiatry at Flinders University; Noel Turnbull, Adjunct Professor in Communications at the Royal Melbourne Institute of Technology; Neil Comrie, former Chief Commissioner of Victoria Police; and Terry Slater, who led the Australian Government’s public health programs before heading up the National Food Authority and the Therapeutic Goods Administration. The sixth community representative position on the board is currently vacant and has been offered to the federal health department. DrinkWise does not advocate for or lobby government in respect of alcohol taxation policy for a very sensible reason — alcohol industry leaders advocating for or agreeing on matters affecting price could constitute a breach of the Trade Practices Act 1974 (Cwlth). DrinkWise programs are strictly evidence-based, drawing on specifically funded high-level independent research executed by leading academics at universities including Griffith, Macquarie, Monash, Deakin, Flinders, and the Hunter New England Institute. Moreover, the DrinkWise “Kids Absorb Your Drinking” advertising campaign was developed through qualitative, quantitative and ethnographic research, as well as the findings of an extensive literature review by child heath experts and academics.2-9 Campaign tracking results show that 28% of adults surveyed in March 2009 reported having reduced the amount of alcohol they drink in front of their children in the previous 12 months. When parents who had seen the DrinkWise advertising were asked about its impact on their drinking behaviour, 39% said they were more self-conscious of how they drink in front of their children, 18% had changed their drinking patterns, and 14% had actually cut down how much alcohol they consume when their children are around.10 DrinkWise Australia: receives funding from the federal government and the alcohol industry for the development of both its evidence base and its programs; has no associations with any international alcohol or tobacco lobby groups; undertakes research through Australian universities to develop the evidence base for its interventions; does not interfere with specification of the research hypotheses, research design and techniques, or publication of results; ensures that the research it funds is undertaken in accordance with the universities’ protocols for conducting independent research; and grants the researchers it funds a “non-exclusive, royalty-free, perpetual license to use, reproduce, adapt and publish Project IP [intellectual property] for research, education, academic and consulting purposes”.11 I was particularly surprised that the letter’s authors would trivialise the importance of education in successful drug intervention programs and instead advocate for increased reliance on supply-side strategies. DrinkWise delivers interventions in a variety of settings, not only through the Kids Absorb Your Drinking campaign, but also through practical tools such as a website (http://www.drinkwise.com.au), information materials and discussion forums, as well as working at the grassroots level with groups such as local government, school organisations, community newspapers, Sports Challenge Australia and the Good Sports program. Educational programs informed by scientific literature, that are implemented and evaluated effectively and not used as a standalone intervention strategy, can work.12 We at DrinkWise hope that anyone with a strong commitment to public health will be able to work with us and not against us. This will ensure that we will be able to continue to run evidence-based initiatives to reduce alcohol-related harm in Australia.

Trish M Worth