Substance‐related disorders

To the Editor: I write in response to the article by Skov on alcohol taxation policy,1 and in the context of the recent defeat of the “alcopops” tax legislation, which is soon to be reintroduced to the Australian Senate. Our democratic political system has held us in relatively good stead, with a reliable system of checks and balances. However, the rejection of the alcopops legislation arguably represents a failure of democracy and a retrograde step for public health, defeating the first Australian public health-centred alcohol tax policy. For this, Senator Fielding and the Opposition should be held accountable. Yes, the tax is not all encompassing, and expansion to broader initiatives, as proposed by Senator Fielding, is not without merit. However, health experts supported the alcopops tax initiative as an important first step, as outlined in Skov’s evidence-based article.1 Skov highlighted the key issues, including that alcohol-related harm is at unacceptable levels, that action is overdue, and that good evidence from Australia and internationally supports taxation and pricing as being among the most effective measures to reduce alcohol consumption and harm.1,2 Overall, the positives of this initiative clearly outweigh the negatives, and defeating it was arguably naïve and ill informed. Historically, both policy and funding are crucial to public health successes. Following awareness of the problem, change must start somewhere, before broadening over time to deliver health benefits (eg, smoking, seatbelts, speeding — all crucial and effective public health campaigns). The most important aspect of the alcopops tax initiative is likely to be that it is a start and a successful avenue to raise revenue. Extension to a full alcohol content-based tax, education, incentives and regulations will come — but much more belatedly now. The defeat of the alcopops tax legislation has threatened this opportunity to significantly contribute to the fight against alcohol misuse. While opposition is by definition the trademark of Opposition parties, bipartisanship should prevail when community benefits are clear. Perhaps more concerning is that a single politician holding the balance of power can disregard history, expert opinion and popular support, and defeat important public health-centred legislation. The manipulation of our political system with the rejection of the alcopops tax legislation was profoundly disappointing. This initiative should not be defeated again. Our politicians should take heed of history, evidence, expert opinion and public sentiment and vote in the nation’s interest to support the alcopops tax legislation on its return to the Senate.

Helena J Teede

There is nothing a government hates more than to be well informed; for it makes the process of arriving at decisions much more complicated and difficult. — John Maynard Keynes, 1938. To the Editor: I would like to contribute to the debate raised by Skov’s timely article1 on the recently defeated “alcopops” tax legislation — the Excise Tariff Amendment (2009 Measures No. 1) Bill 2009.2 Senator Fielding’s requirement for a ban on alcohol industry advertising during sporting events as a condition for his support of the alcopops tax legislation is rational, visionary and affordable from the additional tax raised. Many of the high-profile individual and public health incidents related to alcohol misuse have been among athletes sponsored by the alcohol industry, and around sporting arenas. As the positive outcome of banning tobacco industry sponsorship of sporting events has demonstrated, such bans have at least as strong an impact as would the increased tax on alcopops on reducing exposure of young people to alcohol.3 It is estimated that the alcohol industry contributes up to 23% ($288 million) of the $1.25 billion in annual sports sponsorship in Australia.4 If the government had agreed to Senator Fielding’s prerequisite amendment, and had also fully taken over sports sponsorship responsibilities, it would have achieved two important public health objectives — a reduction in binge drinking and banning of sports sponsorship by the alcohol industry — and would still have had at least $100 million left to address alcohol-related issues; assuming of course that the real objective of the alcopops tax policy was to prevent alcohol-related harm among youths. Had the government agreed to simultaneously ban alcohol industry advertising in sport and maintain the new alcopops tax structure, it would then be on a moral high ground to implement other important alcohol-related public health measures that require no more than strong political will, such as mandated warnings on alcoholic products at the point of sale. In this respect, the French National Cancer Institute’s recent report that alcohol-related colorectal, breast, oesophageal and liver cancer risks increase from one glass per day, and that the consumption of alcoholic beverages of any type is not advised for anyone,5 is instructive.

Niyi Awofeso

To the Editor: Compared with non-Indigenous Australians, Indigenous Australians are more likely to smoke, drink at risky levels and use illicit drugs.1 These alcohol and other drug (AOD) use patterns contribute to or exacerbate a wide range of health conditions and are significant contributors to premature death and morbidity among Indigenous Australians.2 Some attention has been paid to the efficacy of Indigenous-specific AOD programs,3 but there has been little investigation into the capacity of mainstream AOD services to respond to the needs of Indigenous Australians. To address this deficiency, we conducted a national postal survey of workers employed in agencies listed in the 2001 clients of treatment service agencies (COTSA) database. A total of 1345 workers employed in 369 agencies responded (a response rate of 38%). Most respondents (86%) indicated that their agency provided services to Indigenous clients, and that there was either strong (53%) or some (38%) need for such services. However, almost two-thirds (64%) felt that Indigenous clients’ needs were only partially met, and 9% reported that such needs were not met at all. Private sector workers were significantly less likely to report that their agency provided services to Indigenous clients than workers in government agencies and non-government organisations (NGOs) (χ2 = 102.4; effect df = 3; respondents = 1335; P < 0.001). NGO workers were significantly more likely to report a strong need for the provision of AOD services to Indigenous Australians than government and private agency workers (χ2 = 22.2; effect df = 6; respondents = 1110; P < 0.001). Workers in remote locations were significantly more likely to report a strong need for AOD services for Indigenous Australians than workers in other locations (χ2 = 24.9; effect df = 8; respondents = 1108; P = 0.002). Nearly two-thirds of all respondents reported they had no (18%) or limited (44%) access to AOD resources designed specifically for Indigenous Australians. NGO and private agency workers were significantly more likely than government workers to report limited or no access to resources designed to meet the needs of Indigenous Australians (χ2 = 17.8; effect df = 6; respondents = 1168; P < 0.001). These findings indicate a clear need to improve the capacity of mainstream AOD treatment agencies, especially those servicing remote areas, to respond to the needs of Indigenous Australians. Until improvements are made, AOD problems will continue to erode the health and wellbeing of Indigenous Australians, with predictable outcomes in relation to injury, mental health, parenting and contact with the criminal justice system. As recently highlighted by Indigenous spokesperson Mick Dodson,4 initiatives, beyond support for Indigenous workers and communities, are required to improve mainstream services for Indigenous clients in a culturally sensitive and appropriate manner.

Ann M Roche · Kenneth J Pidd · Vinita Duraisingam

Evidence shows that cost does affect alcohol consumption, and reducing consumption improves public health There is strong evidence that increasing the cost of alcohol reduces the overall amount that is consumed.1 In a range of countries, price increases have been consistently shown to reduce alcohol consumption and related harms in both the general population and at-risk populations such as young people and heavy drinkers. Conversely, price decreases have resulted in an increase in consumption and harm.1-3 In this context, the Australian Government’s April 2008 increase in excise tax (Bill introduced on 11 February 2009) on ready-to-drink (RTD) spirit-based products (RTDs; “alcopops”) is an evidence-based strategy to reduce excessive RTD consumption among young people. The alcoholic content of RTDs is now taxed at a similar rate to that of other spirits (tax increased from $39.36 to $66.67 per litre of pure alcohol). Critics have argued that the RTD tax increase has not reduced alcohol consumption by young people, and will not do so. One claim is that young people will merely switch to other beverages. These arguments have been made by some from the alcohol industry and some researchers. Doran and Shakeshaft, for example, argued that young people “ seem to be price inelastic about their alcohol demand”.4 Citing a national school survey, they claimed that “spirits are by far the beverage of choice for the 45% of 16–17-year-old Australians who drink, despite spirits being the most highly taxed beverage in Australia, and the most expensive per litre of alcohol”. This is not evidence for price inelasticity. They also argued that “overall rates of usual or binge consumption in Australia are unlikely to substantially fall, because spirits hold a smaller market share than beer, and young people will more than likely switch their preference”.4 The weight of scientific evidence suggests otherwise — that overall consumption is likely to decline because young people’s demand for alcohol is elastic.1-3 The survey series on which Doran and Shakeshaft rely shows that beverage preferences vary between boys and girls and over time. In 1999, before reductions in tax and in the retail price of RTDs in 2000, RTDs were the preferred beverage of about 23% of 12–17-year-old female drinkers. By 2005, after the tax decrease, 48% of young females drank RTDs, while the preference for higher-taxed spirits fell from 42% to 30%. For 12–17-year-old males, RTD consumption increased from 6% to 14%, a small share compared with spirits (39%) and beer (33%).5 Although new products and marketing strategies may have contributed to this substantial change, these data suggest that young Australians, like their counterparts in other countries,2 do alter their beverage choices in response to price changes. Definitive statements about the impact of the “alcopops tax” are premature in the absence of independent alcohol sales data. It is regrettable that there are no readily available, official monthly sales data for all alcoholic beverages, like those obtained by the detailed monitoring that we know is conducted by private industry.6 However, available evidence does indicate that the tax has reduced sales of RTDs and the reduction was far from wholly offset by a switch to other beverages. A market research company that regularly compiles reports on sales of alcohol products has estimated national monthly sales of packaged alcohol (sold for off-premises consumption by liquor licensees across the five mainland states of Australia) by beverage type for 2007 and 2008 ().7 These data show that in the 3 months after the April 2008 tax increase, 91 million fewer standard drinks were sold as RTDs than in the same months in the previous year. Standard drinks sold as spirits and beer increased but wine sales decreased. The increase in spirit and beer sales (48 million standard drinks) was only 53% of the 91 million fewer RTD drinks sold. A decline in RTD sales was also reported on the basis of Australian Tax Office data. These showed a 54% reduction in sales of RTDs and a 7% increase in spirit sales from April to June 2008.8 In presenting the Excise Tariff Amendment Bill to Parliament, the Minister for Health and Ageing confirmed that: “Tax office figures drawn from the first nine months of this measure show that alcopops sales have dropped by 35 per cent compared to the previous year”.9 Critics have been hasty in predicting that young people’s drinking would be unresponsive to the RTD tax increase. In keeping with a large body of research evidence, the early indications are that RTD sales declined in the first few months after the tax increase. Previous research suggests that this decline in alcohol sales (a reliable proxy for consumption10) will produce a public health benefit.1-3 Further investigation is needed to determine specifically in which population group(s) the benefit accrues; for example, whether this reduction in RTD purchases occurred primarily among young drinkers (the target of the tax increase), and what other factors may have contributed to the reduction. Informed policy debate requires independent evaluations of short-term and long-term effects of these tax changes on consumption and harm indicators (eg, injuries). Nevertheless, the evidence to date is that the “alcopops” tax is a step in the right direction. Number of standard drinks* consumed in May to July, 2007 and 2008, by beverage type Beverage type Million standard drinks consumed Difference in million standard drinks % Change 2007 2008 RTDs 348 257 − 91 − 26.1 Beer 886 899 13 1.5 Wine 797 776 − 21 − 2.6 Spirits 313 348 35 11.2 Total 2344 2280 − 64 − 2.7 Source: Nielsen Liquor Services Group (NLSG) 2008.7 RTDs = ready-to-drink spirit-based products. * One standard drink = 10 g pure alcohol. To accurately convert beverage volumes to pure alcohol, the NLSG applies alcohol conversion factors at the subsegment level for beer (eg, regular, mid-strength, low-strength beer) and RTDs. Average alcohol contents by beverage type: RTDs 5.0%; beer 4.8%; straight spirits 38.0%; and wine 13%.

Tanya N Chikritzhs BA(Hons), PostGradDip(Epi · Paul M Dietze BSc(Hons), PhD · Steven J Allsop BSc, PhD · Michael M Daube BA(Hons), HonDSci · Wayne D Hall BSc(ApplPsych), PhD · Kypros Kypri BA(Hons), PhD

The effects of cannabis use on health and social adjustment are profound Substance misuse by Indigenous people has long been recognised as one of the devastating consequences of contact with Western culture. Misuse of tobacco, alcohol and petrol among Indigenous Australians has received much attention. Cannabis, by contrast, has not been viewed as a major problem. But since the 1990s, it has become apparent that heavy cannabis use is common in some remote Indigenous communities.1 The associated health and social burdens are now being recognised.1,2 Indigenous Australians, whether living in urban or rural settings, are more likely than other Australians to report cannabis use.3 Recent reports suggest that cannabis use is also relatively high among Indigenous populations in New Zealand, Canada and North America.4 Limited data are available on patterns of cannabis use among Indigenous Australians.3 However, a recent 5-year study of adolescents and young adults in three remote communities in Arnhem Land in the Northern Territory has found that not only is cannabis use common in remote Indigenous settings, but its effects on health and social adjustment are profound.4-6 These three communities are close to one another but very isolated, being over 550 kilometres from the nearest city. There is one local Indigenous language, and English is a secondary language. Tobacco use was found to be the norm in these communities, with over 90% of adolescents and young adults smoking.7 Because of restricted access to alcohol, problem drinking was uncommon.7 In contrast, cannabis use was endemic, with over 70% of males and 20% of females being current users.5 Cannabis was typically consumed mixed with tobacco and smoked using a locally fashioned “bucket bong” that gives the user a rapid and intense dose with little smoke lost.5 Regular heavy use (≥ 6 “cones” daily) was found in almost 90% of users.7 This is around twice the consumption of regular cannabis users elsewhere in Australia.1 Furthermore, about 90% of the Indigenous users reported symptoms of cannabis dependence.1 This compares with about 20% of users aged 18 or over in the general Australian population.3 Of even greater concern was a suggestion that, for most Indigenous users, cannabis was not a passing adolescent phase. After 5 years of follow-up, the great majority reported continuing heavy use.4 Cannabis use was linked to substantial health problems and social burdens in these communities, which are already disadvantaged by isolation and poverty.2,5,8 Up to 10% of the communities’ total income and between 31% and 62% of a user’s median weekly income was spent on cannabis.5 Cannabis users were less likely than non-users to participate in education or training5 and more likely to report auditory hallucinations, suicidal ideation,6 symptoms of depression,7 and having been imprisoned.6 Community violence increased when cannabis supplies were scarce.1,2 The effects on traditional life were described by one NT Indigenous mental health clinician in the following way: Too many of my people are chained to [cannabis]. They don’t go out hunting or spend time by the river with their family. They just sit and smoke [cannabis], then look for money to buy more [cannabis] and get into fights when they can’t get any (Muriel Jaragba, personal communication). What accounts for the unusual patterns of cannabis misuse in these remote Indigenous communities? There is little evidence that cannabis is grown locally,9 but much anecdotal evidence that market networks supplied by dealers based in urban or regional centres are extensive and resilient, making cannabis readily available (A R C, unpublished observation). Alcohol restrictions have been effective in reducing problem drinking within communities, but may have had the undesirable consequence of encouraging an increase in cannabis use where it could be easily obtained.5 As with risks for other forms of substance misuse in these communities, the social context is important. Limited employment and education opportunities; crowded, poor-quality housing; community-wide feelings of disempowerment; and grief and loss related to high mortality, morbidity and incarceration rates are all likely risk factors for substance misuse. Cannabis misuse is likely to be both a consequence of this type of social disadvantage and a perpetuating influence. Cannabis misuse in remote Indigenous communities has been overlooked for too long. It is now clear that it is yet another major problem for these already disadvantaged communities, with evidence of cannabis misuse across a broad area of northern Australia.1,2,9 As well as in the NT, concerns about the level of cannabis use have recently been noted in Cape York8 and anecdotally in other parts of remote and regional Australia. Further research is needed to investigate the impact of cannabis use on urban Aboriginal and Torres Strait Islander Australians. Effective responses will not be easy. Controls on supply by state- or territory-based police are one of the few available measures.6 In order to be effective, policymakers and service providers would need to work collaboratively with local communities to tie in local prevention and treatment initiatives with existing supply control initiatives. Such programs would need to use Indigenous language and cultural frameworks, build capacity of local Indigenous professionals, and improve understanding of the harms associated with cannabis misuse.10 Ultimately, tackling the misuse of cannabis and other substances in remote settings will depend on creating opportunities for social development and for continuing education, training and employment of adolescents and young adults.

K S Kylie Lee BMus(Hons) · Katherine M Conigrave FAFPHM, FAChAM, PhD · George C Patton MD, FRANZCP · Alan R Clough PhD

Scattered: the inside story of ice in Australia. Malcolm Knox. Sydney: Allen & Unwin, 2008 (xi + 290 pp). ISBN 978 1 74175 358 5. Malcolm Knox is a Walkley Award-winning journalist and he has a keen grasp of both the pharmacology and psychiatric effects of crystal methamphetamine. Scattered provides a lucid, elegant description of the turbulent recent history of ice in Australia. Knox goes beyond the statistics and includes a series of case vignettes, exploring the human cost of this drug in the Australian context. Knox explains that the heroin drought in Australia since 2000 has led to an alternative, yet far more damaging, drug supplanting the somnolent effects of the opioids. Ice is relatively cheap, hitting the streets in all our capital cities (and everywhere a truck goes), and provides an instant, profound teeth-grinding hit, far more potent than any other methamphetamine in history. This book is a roller coaster read in three sections: going up, the high, and coming down. In many ways, the book’s structure follows the effects of this most potent psychostimulant on many unfortunate users. Many patients that I have seen in my addiction practice have suffered severe drug-induced ice psychoses requiring urgent hospitalisation and larger than usual doses of tranquilliser medication. Such patients are alarming to both doctors and nursing staff alike. Practitioners at the coalface can only hope that ice becomes less popular and that we are spared the prospect of such violent psychosis or a terrified patient hiding under a desk, paranoid about imaginary helicopters spying on his every move. This book will not be to everybody’s taste because of the graphic descriptions of ice-fuelled violence and sexual depravity, but it should be required reading for all doctors who encounter such patients on the edge of oblivion.

Raymond C Seidler

On speed: the many lives of amphetamine. Nicolas Rasmussen. New York: New York University Press, 2008 (ix + 351 pp). ISBN 978 0 8147 7601 8. Amphetamines are highly topical in the Journal — recent articles have discussed the controversies of prescribing them for attention deficit hyperactivity disorder, and their associations with violence in emergency departments and criminal offending. This book situates current concerns about stimulant use in a historical context and, in doing so, crosses swords with the pharmaceutical industry. But Rasmussen also has insights into the past roles of military medicine and social concerns that might be exploited to increase market share for drugs that are sold for “aspirational” goals. The author’s background is in history and philosophy of science. His book is at times irritating, particularly with repeated and unconvincing efforts to calculate past consumption of stimulants in the United States. These quibbles are minor, however, for the scope of his work is provocative and applicable to other areas in which social mores and medicine interact. His premise — that amphetamines have been marketed and remarketed for dubious indications and social woes, rather than for medical problems — is appealing and his research painstaking. However, most intriguing is the discussion of marketing, of efforts to rebrand addiction as habituation, and of the evolution of life problems seen as warranting psychopharmacological intervention. Rasmussen makes a good case that patent medicines and their promises have been supplanted by amphetamines and related drugs. This is a well referenced and easily read book, which reminds the reader that uncritical acceptance of drug marketing is unwise. The book is not as tendentious as the works of David Healy or Peter Breggin, and for that is all the more compelling. Nevertheless, any doctor will be challenged by the ease with which novel drug indications are accepted and by the shifts in prescribing patterns, which remain so similar. Moral panics about drugs are reinvented by every generation, and Rasmussen admirably provides the historical setting for current anxieties about stimulants. Melbourne, VIC

Danny H Sullivan

To the Editor: In their recent case series, Lintzeris and colleagues state that the symptoms leading to hospital presentation were “associated” with naltrexone implants.1 In half of the 12 cases, the symptoms were related to the induction of withdrawal rather than the presence of naltrexone — an important distinction that may not be apparent to all, but of which the authors would be aware. Three of the remaining cases reflect the complexities of pain management in patients being treated with naltrexone, which are not restricted to those with implants. This dilemma is also encountered in patients taking buprenorphine. Patient 8 had an anxiety disorder, and his symptoms probably related to an absence of opiate; and Patient 9 had symptoms that were probably due to cocaine use. Abstinence is a patient’s choice, and naltrexone can be effective in minimising the risks associated with the consequent lowered tolerance to opioids.2 I am concerned that undue emphasis appears to have been placed on the association of adverse outcomes with implants, with such statements as: “This case series identifies severe adverse events associated with the use of naltrexone implants”. In fact, the causal condition is usually the induction of opiate withdrawal rather than the presence of a naltrexone implant.3 The statement that “Most of these cases (8/12) can be attributed to the naltrexone implant or implantation procedure” is true, but it would be more appropriate to acknowledge that the procedure appeared to be the cause in most cases and that only in one case (Patient 7) could the implant be conclusively implicated. It is not appropriate to refer to difficulties in pain management as “severe adverse events”, as the blockade of the μ opioid receptor is the reason naltrexone is used. In addition, it is important to note that a trial of injectable naltrexone has shown promising results.4 While these facts are acknowledged by the authors, their emphasis on the association of adverse events with the presence of a naltrexone implant, rather than demonstrating causality, is concerning. Similarly, this approach appeared in Gibson and colleagues’ earlier commentary on overdose deaths in patients with naltrexone implants.5 Nonetheless, I commend the authors for raising the issues relating to the need to examine the role of naltrexone implants in treating opioid dependence and exploring alternatives to the use of rapid detoxification. I also endorse the need for thorough assessments, treatment planning and evaluation in patients undergoing such therapies.

D Martyn Lloyd-Jones

To the Editor: We read with interest the report of 12 hospital presentations related to the use of naltrexone implants.1 The accompanying editorial highlights how the rigorous scrutiny required to evaluate the efficacy and safety of this procedure is lacking.2 Regrettably, this study is likely to distort rather than inform the debate. Lintzeris and colleagues1 only identified patients with naltrexone implants who were referred to the Drug and Alcohol Consultation–Liaison services, not all patients presenting to the study hospitals. Additionally, the authors did not follow the methodology of chart reviews, as recommended by Gilbert and colleagues.3 Four of the 12 patients clearly had problems unrelated to their naltrexone implants. There was no attempt to identify the number of naltrexone implantations performed (ie, the denominator), nor was there any attempt to compare the naltrexone group with others being treated with agents such as methadone or buprenorphine. In 2003, we published our experience of naltrexone-accelerated detoxification in the emergency department (ED) of Sir Charles Gairdner Hospital.4 The hospital’s clinical toxicology service is based in the ED, and the hospital is located 2 km from the only private clinic in Perth that was using naltrexone during the study period in 2001. Working collaboratively with this clinic, patients developing complications from detoxification were referred to our service. In 6 months, 42 patients (7% of all those receiving naltrexone treatment) presented to the ED — 17 within 24 hours of treatment and 31 within 48 hours. Gastrointestinal symptoms of withdrawal were present in 18 patients, and central nervous system symptoms of withdrawal (predominantly agitation) in 14. Two patients required intubation for airway compromise secondary to a combination of agitation and chemical sedation. In 23 patients receiving naltrexone implants (rather than oral therapy), three developed infections and three complained of local pain. The mean length of stay for all patients was 18 hours (compared with 2.3 days in Lintzeris et al’s study), with the longest stay being 92 hours for one of the patients admitted to the intensive care unit. During the study period and the subsequent 6 months, four deaths of individuals who had undergone naltrexone-accelerated detoxification were reported to the Coroner, all being classified as probable drug overdose, probably opioid. None of these patients had presented to the hospital’s ED during the study period. It is important that good data are made available to inform the debate on naltrexone implants in the management of opioid dependence. Better communication and collaboration between clinics using naltrexone, EDs, and alcohol and drug services will improve the care of these patients.

Mark Little · Lindsay M Murray

To the Editor: The study by Lintzeris and colleagues1 and the associated editorial2 criticise naltrexone implants. However, the study is replete with errors regarding the 12 cases reported. A key to successful rapid opioid detoxification (ROD) is octreotide. An agonist of non-μ gut receptors, it prevents gastrointestinal symptoms of withdrawal.3,4 Earlier aggressive dosing is more effective. Only two of the six patients reported as having precipitate opiate withdrawal received octreotide, administered in both cases by their local doctor. Presumably this doctor performed the ROD. Why was the octreotide administration not repeated? Patient 7 was reported as having a localised abscess at the implant site. These may arise a variable period after implant insertion. Magnesium-monostearate, used as a binder in naltrexone and many other implants, may liquefy, resembling pus. Results of repeated microbiological examination are always negative. An actual infection at the implant site is rare. Patient 8 demonstrates that many patients use opiates and other drugs as self-medication for their psychiatric symptoms. It is regrettable that this patient’s psychiatrist was not involved in the decision making. Was the doctor doing the ROD aware that there was a psychiatrist involved? Transient psychosis may occur following ROD; use of antipsychotics is appropriate. Arrhythmias (as diagnosed in Patient 9) are a textbook in themselves. Pre-ROD preparation requires assessment for comorbidities including bacterial endocarditis and arrhythmia syndromes. Substance-misusing patients often use arrhythmogenic agents such as amphetamine. No mention was made of precipitate withdrawal symptoms in this patient, so an electrolyte abnormality is unlikely. Patients 10–12 had problems that were unrelated to the naltrexone implants and poorly managed by the receiving hospital. Naltrexone has 2 log the affinity for opiate receptors to that of morphine and most other opiates.5 This means that 1 mg of naltrexone will block 1 g of another opiate. Using opiates to treat patients in these circumstances therefore makes no sense. Ketamine, local anaesthetic blocks, paracetamol and non-steroidal anti-inflammatory drugs are alternative options for treatment. To compare naltrexone implants with thalidomide2 is emotive; all the components of the implants are approved agents. Similarly, to say they have not been fully tested is to condemn all products supplied by compounding pharmacists. Testing of serum naltrexone levels (to assess whether an implant is still working) is not rebatable under Medicare, so is expensive to perform. Research is a necessary component of naltrexone implants, and I would happily cooperate with any of the study authors in coordinating and performing such research.

Michael P W Kozminsky

To the Editor: A recent article by Lintzeris and colleagues,1 ostensibly about naltrexone implants, actually has little to do with implant treatment. Only one of the 12 reported cases involved problems linked specifically to naltrexone (antagonist) treatment being administered in implanted rather than oral form. This case involved infection at the implant site — undesirable, certainly, but about as noteworthy as the occasional infections that occur after abdominal surgery or breast implantation, despite antibiotic prophylaxis and careful technique. The remaining 11 admissions reflected not implant use but either the procedure of rapid antagonist induction (RAI) or the desired pharmacological effects for which naltrexone was prescribed in the first place (and one admission for unrelated pneumonia). RAI is needed because conventional antagonist induction requires complete opiate withdrawal before starting naltrexone. As true conventional withdrawal completion rates, even with inpatients, are typically below 30%,2 conventional techniques will typically achieve only derisory naltrexone induction rates. Various forms of RAI or accelerated induction, with induction rates typically around 100%, are more effective and more cost-effective.3,4 Similarly, complaining that pain management is difficult in naltrexone patients is like complaining that patients being treated with anticoagulants bleed or bruise more after surgery or injury. Fortunately, effective non-opiates (notably subanaesthetic ketamine) exist. The acute post-RAI problems seen in this case series would have been identical had every patient undergone RAI to oral rather than implanted naltrexone. Indeed, while 150 mg orally could block opiate analgesia for up to 72 hours, implants produce low but consistently effective naltrexone levels, disappearing within hours of implant removal, should that be unavoidable. I agree, however, that RAI clinics should optimise immediate post-RAI management. A recent conference featured the first presentations of the first four randomised controlled trials of implanted naltrexone. Three showed statistically and (more importantly) clinically significant advantages over “as usual” post-withdrawal treatment,5 or over oral naltrexone and placebo implants.6,7 The fourth,8 comparing implants with methadone maintenance in pre-release prisoners, had only modest statistical power (n = 21), but implant patients had less dropout and used about 50% less heroin. We already know that long-acting implants can largely prevent the opioid overdoses that are otherwise an intrinsic and sometimes lethal hazard of all abstinence-based programs;9 and that all implants prevent the otherwise high relapse rates typical of the first 4–6 weeks after detoxification.10 Surgeons, I am shocked to discover, have been using anaesthesia for 162 years without a comparable placebo-controlled evidence base.

Colin L Brewer

In reply: Our case series1 aimed to alert health practitioners to the types of hospital presentations associated with naltrexone implants and issues in managing such patients, particularly as these have not been well documented in the medical literature. These letters appear critical of any such communication. We maintain that our article1 identifies important clinical issues — such as the difficulties of providing analgesia in patients with implants of uncertain duration of effect (whereby the treating hospital staff have no way of knowing whether the implant is providing “active” plasma levels of naltrexone, given the lack of a licensed product). Ultimately, our study could not hope to provide the type of data that can only be accurately determined by independent clinical trials — such as the incidence rate of serious adverse events (as suggested by Little and Murray) or how these are most effectively managed (eg, the role of octreotide compared with ondansetron for managing protracted vomiting, as suggested by Kozminsky). A key complaint from the correspondents is whether the serious adverse events of opiate withdrawal and dehydration were caused by the naltrexone implant or by the rapid opioid detoxification process that accompanied the implant’s insertion. We acknowledged the difficulty of attributing causality in our article, but, unlike the correspondents, we cannot dismiss the possibility that the naltrexone implant may have contributed to the severity or duration of the opiate withdrawal syndrome. Clearly, there is a pharmacological basis as to how the presence of naltrexone from an implant may contribute to opiate withdrawal in a recently detoxified individual. Research comparing rapid opioid detoxification plus a naltrexone implant with conventional detoxification plus a naltrexone implant is required, to allow an assessment of whether naltrexone implants themselves contribute to the incidence, severity or duration of any opiate withdrawal. Until such data exist, it is appropriate to associate opiate withdrawal with naltrexone from the implants. We concur with several of the correspondents that further research is required to address many of the issues raised by our study, as well as better communication between service providers, better procedures for management of complications, and better assessment and patient selection. We maintain that naltrexone implants should not be routinely used until research has demonstrated their safety and efficacy, and, importantly, until there is a licensed naltrexone implant product with appropriate regulatory safeguards for patients and providers.

Nicholas Lintzeris

Australia should be improving, not abandoning, the collection of alcohol sales data Australians pay a substantial price for the pleasure they derive from alcohol. According to the latest estimate, on a net basis, alcohol accounts for 2.2% of the total disease burden in Australia.1 This is marginally more than illicit drugs (2.0%),1 but alcohol’s toll would be even higher if the 3430 deaths of young adults caused by alcohol-related road crashes, accidents, assaults, suicide and other causes were not partially offset by 2345 deaths from heart disease counted (some would argue erroneously)2,3 as having been averted by moderate drinking in adults over the age of 65.1 The health costs of risky alcohol use are not the only social costs. According to a National Drug Strategy study,4 in addition to $1.98 billion in health costs in the 2004–05 financial year, alcohol misuse cost the Australian economy $3.58 billion in lost productivity in the workplace, $1.57 billion in lost productivity in the home, $1.61 billion in crime-related costs, and $2.20 billion in road accidents, with a total social cost in excess of $15 billion. For the past decade, illicit drugs have overshadowed alcohol as a political and public health issue. Policies to reduce alcohol-related harms (such as taxation and reduced trading hours)5 have been effectively opposed by an alcohol industry that has had the ear of federal and state governments, both of which have major conflicts of interest in alcohol policy. The federal government derives substantial income from alcohol excise, while state and territory governments impose licensing fees and taxes on gambling in pubs and clubs. Governments are also aware that the alcohol industry plays an important role in the Australian economy, especially in regional areas (eg, the wine industry in South Australia). The recent change of federal government has brought a renewed policy interest in alcohol use. The alcohol industry claims that this interest is misplaced, citing data which suggest that per capita alcohol use and frequency of consumption, as indicated by household surveys, have been relatively stable for over a decade.6,7 However, there are doubts about the quality of these alcohol trend data, and the most recent survey data certainly indicate there is cause for concern. In 2007, one in five Australians over the age of 14, including nearly half (44%) of young men and around a third of young women aged 20–29 years, reported drinking in risky ways monthly or more often.7 The alcohol industry derives substantial profits from risky drinking, with — on conservative estimates — two-thirds of all alcohol, and 80% of alcohol used by young people aged 14–24 years, consumed in ways that put the drinker’s (and others’) health at risk.6 It is essential that debates about alcohol policy are informed by good data on alcohol use and alcohol-related harm in the Australian population.8 The World Health Organization has recommended that public health monitoring of alcohol use should include credible estimates of per capita alcohol consumption derived from alcohol sales data, in addition to well conducted population surveys of drinking patterns.8 Despite this, Australia is now in danger of failing to collect alcohol sales data at a time when community concern about alcohol is increasing and the quality of survey data may be declining. For many years, the Australian Bureau of Statistics (ABS) has published national estimates of per capita alcohol consumption9 based on import clearance, excise and domestic alcohol sales data. Until 1997, the ABS estimates were complemented by state and territory alcohol sales data collected by liquor licensing authorities. However, after a High Court ruling that state liquor licensing fees were unconstitutional, most jurisdictions stopped collecting these data; only Western Australia and the Northern Territory continue to do so.6 In its most recent report, the ABS has indicated that it may no longer report on national alcohol consumption estimates derived from sales data.9 If this were to happen, Australia would be the only OECD (Organisation for Economic Co-operation and Development) country to not collect national alcohol consumption data. The collection of alcohol sales data should be improved rather than abandoned. Without these data, policymakers, community action groups and public health researchers would lack essential information to monitor trends in per capita alcohol use, which is strongly related to adverse health outcomes such as liver cirrhosis, motor vehicle crashes, and suicide.5 National sales data are essential for monitoring trends in per capita consumption, and they facilitate studies of the relationships between changes in the level of per capita alcohol consumption and both population health outcomes and social harms (eg, arrests for assault and public disorder).5 Sales data also provide a benchmark to gauge the accuracy of national alcohol consumption surveys.10 Household surveys of self-reported alcohol use, such as the National Drug Strategy Household Surveys and the National Health Surveys, provide important information on drinking patterns among population subgroups, but, at best, they complement rather than substitute for sales-based data. For example, the National Drug Strategy surveys and the National Health Surveys are conducted every 3 years and 5 years, respectively, and the alcohol use they measure accounts for only about 60% of the alcohol that is sold.10 The response rates of the most recent National Drug Strategy surveys (in 2004 and 2007) have been less than 50%, raising concerns about the representativeness of survey data for population alcohol use. State and territory sales data should be collected in ways that enable the sales volumes of each beverage type to be estimated at local levels. These local-level sales data can be used to evaluate the effectiveness of community initiatives to reduce alcohol-related harm, such as those in northern and central Australia, and the effects of liquor licensing changes on alcohol consumption. State-level data could be used to evaluate the effect of new alcohol management strategies such as pub “lock outs”, restrictions on types of alcohol that can be sold in Aboriginal communities, and the tax increase on premixed spirits-based drinks. The collection and reporting of alcohol sales data would entail minimal cost to the alcohol industry, which already provides these data to commercial market research companies. Given that alcohol harms a substantial proportion of people who use it and can also adversely affect the safety and amenity of those who do not misuse it, the federal government should require alcohol sales data to be provided by those who are licensed to sell this intoxicating and addictive commodity.

Wayne D Hall BSc, PhD · Tanya N Chikritzhs BA(Hons), GradDipEpidBioStats, PhD · Peter H N d’Abbs BA, MA, PhD · Robin G W Room PhD

To the Editor: We read the article by Bunting and colleagues1 with interest, as it attempted to address the important question of whether agitation and aggression are more commonly seen with methamphetamine toxicity. However, we have several concerns about the results presented in this study and the conclusions drawn by the authors. First, while they have shown that methamphetamine users were more likely to be agitated and aggressive than patients in other “toxicology-related presentations”, this is not surprising. The most common “toxicology-related presentations” to emergency departments are deliberate self-poisonings with drugs like paracetamol, non-steroidal anti-inflammatory drugs, and benzodiazepines,2 and these agents do not cause significant agitation. The control group in the study by Bunting and colleagues should have been patients presenting with toxicity associated with other recreational drugs. Second, the real issue is whether agitation and aggression are more common with methamphetamine than with other sympathomimetic agents, such as cocaine, amphetamine and methylenedioxy-methamphetamine, as well as ketamine. The authors should therefore have compared patients in methamphetamine-related presentations with those presenting with toxicological symptoms related to this group of drugs, which have also been shown to be associated with significant aggression.3,4 Third, the authors have not stated how they determined whether the presentation was related to methamphetamine or other drugs. It must be assumed that this was on the basis of patients’ self-report. Patients could potentially have been miscategorised without appropriate confirmatory toxicological screening. Fourth, the authors made no comment on the effect of ethanol co-ingestion and the risk that this can precipitate violence and aggression, which could be a considerable confounding factor. Previous authors have reported that violence and aggression are more commonly associated with ethanol ingestion than with use of other recreational drugs.4 Finally, we are concerned that the conclusion of their abstract is not backed up by the results of their study, as there are no data presented to support their statement that “methamphetamine appeared to be used consistently, rather than as an episodic ‘party drug’”. We therefore urge that clinicians interpret the results of this study with caution.

Paul I Dargan · David M Wood

To the Editor: We concur with Chan and Sullivan regarding the importance of targeting modifiable risk factors, such as smoking during pregnancy, to improve perinatal outcomes.1 Alcohol consumption during pregnancy is another important modifiable risk factor. Alcohol exposure in utero is associated with growth retardation, birth defects, and impaired development and neurological function. Individuals exposed to alcohol in utero may have lifelong medical and psychosocial problems.2 In our national survey of 1103 Australian women aged 18–45 years conducted in 2006, 34.2% of women reported that they had consumed alcohol during their most recent pregnancy and 16.2% had smoked. When asked whether they would consume alcohol or smoke if they were to become pregnant in the future, 23.7% said they would consume alcohol and 4.0% said they would smoke. Intention to smoke during a future pregnancy was significantly associated with intention to consume alcohol (odds ratio, 5.1 [95% CI, 2.7–9.4]; P < 0.001).3 This strong association suggests that strategies aimed at reducing smoking and alcohol consumption during pregnancy should target both behaviours. Chan and Sullivan also note the need for uniform national data on smoking during pregnancy. Although alcohol consumption is more common than smoking during pregnancy, fewer data have been collected and reported on alcohol consumption during pregnancy than on smoking. Five Australian states and territories collect data on maternal smoking status,1 and the data are published by the Australian Institute of Health and Welfare in their annual Australia’s mothers and babies report.4 In contrast, data on alcohol consumption during pregnancy are routinely collected by only three states and territories (Tasmania, the Australian Capital Territory and the Northern Territory). These data are minimal and inadequate for monitoring trends or evaluating the effectiveness of public health interventions. Smoking and alcohol can both cause preventable harm to the unborn child. Public health strategies, national uniform data collection and community education are required to address these issues in order to promote healthy pregnancies and healthy babies.

Elizabeth M Peadon · Carol I Bower · Elizabeth J Elliott

To the Editor: We report significant sinus bradycardia in a patient presenting with an acute coronary syndrome shortly after beginning bupropion therapy to assist with smoking cessation. A 53-year-old man was attended by paramedics for typical ischaemic chest pain. He had sinus bradycardia (45 beats/min) and hypotension (blood pressure, 85/60 mmHg), and was found to have a serum troponin I concentration of 1.2 μg/L, but no diagnostic electrocardiographic changes. He was admitted to our hospital with an acute coronary syndrome. He reported his medications at the time of admission as including metoprolol 50 mg twice daily (for hypertension) and paroxetine 20 mg daily (for depression). The patient was given multiple doses of intravenous atropine (total, 1.2 mg) and adrenalin (total, 2 mg). After an adrenalin infusion was begun, he developed ventricular tachycardia (170 beats/min), but his cardiac rhythm spontaneously returned to sinus bradycardia. Two days after admission, two coronary stents were successfully deployed in a critically stenosed right coronary artery. Bradycardia (45–50 beats/min) persisted. The following day, it was discovered that 3 weeks previously, the patient’s general practitioner had prescribed bupropion 150 mg twice daily to assist with smoking cessation, which he had been taking up until the day of admission. Bradycardia continued until hospital discharge. One month after discharge, he was in sinus rhythm (60 beats/min) and was clinically well. Bupropion is a selective noradrenalin, dopamine and serotonin reuptake inhibitor. The mechanism by which it enhances the ability of patients to abstain from smoking is unknown.1 Bupropion inhibits the activity of the cytochrome P450 2D6 isoenzyme, which metabolises metoprolol.2 Concurrent use of bupropion and metoprolol can increase serum metoprolol levels, and clinically significant bradycardia has been reported.3 Further, paroxetine, a selective serotonin reuptake inhibitor (SSRI), is a potent cytochrome P450 2D6 inhibitor, which would have further increased serum metoprolol levels. Bradycardia associated with metoprolol and paroxetine dual therapy has been described.5 Additionally, there is the potential for serotonin syndrome to develop in a patient administered multiple SSRIs. In our patient, the administration of bupropion and paroxetine could have potentially led to serotonin syndrome.6 Our patient’s pharmacological profile was complex, with potential adverse pharmacodynamic effects. The most likely precipitant of the patient’s bradycardia was his acute coronary syndrome, although bupropion may have contributed. The case highlights the potential for significant drug interactions when new drug therapies are initiated. Bupropion and metoprolol (and other drugs metabolised by the cytochrome P450 2D6 isoenzyme pathway) should be co-administered with caution. The importance of common pathways of drug metabolism should be recognised to avoid potential adverse events, particularly when multiple medications are used.

Jacqueline Landau · Andrew E Ajani

Addiction medicine deals with problems arising from the use of psychoactive substances, and encompasses the disciplines of general practice and primary care, psychiatry, psychology, internal medicine, public health, pharmacology and sociology. Addiction is a chronic, relapsing illness that is difficult to cure. There are now effective, evidence-based interventions for the prevention and treatment of substance misuse disorders. Harm minimisation and treatment are more cost-effective than policing and supply-reduction methods of responding to substance misuse.

Brian R McAvoy MD, FAChAM, FRNZCGP

Objective: To examine the nature and extent of ambulance attendances involving γ-hydroxybutyrate (GHB) and to compare these with heroin-related attendances in Melbourne, Victoria.Design: Retrospective analysis of a database of ambulance service records on attendances at non-fatal drug overdoses, March 2001 – October 2005.Participants and setting: Patients who took GHB and were attended to by an ambulance, as recorded by Metropolitan Ambulance Service (Melbourne) paramedics.Main outcome measures: Transportation to hospital by ambulance; other outcomes included number, age, sex and Glasgow Coma Score (GCS) of patients, characteristics of attendances (in public or private space, others present, police co-attendance).Results: There were 618 GHB-related ambulance attendances across the 46 months of data collection; 362 involving GHB only and 256 involving the concurrent use of GHB and other drugs. These figures compare to 3723 heroin overdoses observed during the same period. The number of GHB-related attendances increased by around 4% per month, which was a higher rate of increase than that found for heroin overdose attendances. Most patients were younger than 25 years, were attended in public spaces, and had a GCS < 10. Around 90% of patients were transported to hospital, compared with 21% of heroin overdose attendances.Conclusions: Ambulance attendance data can be used to index GHB-associated harms. The clear increases in GHB-related ambulance attendances over time highlights the need for further research on how best to respond to this emergent drug-related harm.

Paul M Dietze PhD · Stefan Cvetkovski MPH · Monica J Barratt BSc(Hons) · Susan Clemens MPH

Objective: To determine the extent to which depressive symptoms are associated with heavy cannabis use in an Aboriginal population in Arnhem Land, Northern Territory.Design, participants and setting: Cross-sectional study involving interviews with 106 Indigenous participants (57 males, 49 females) aged 13–42 years in three remote Aboriginal communities in Arnhem Land, NT, Australia.Main outcome measures: Measures of depressive symptoms (a raw score of ≥ 6 out of a possible 18 on a modified version of the Patient Health Questionnaire-9) and self-reported heavy cannabis use (six or more cones daily).Results: After adjusting for other substance use (tobacco, alcohol and lifetime petrol sniffing), age and sex, heavy cannabis users were four times more likely than the remainder of the sample to report moderate to severe depressive symptoms (odds ratio, 4.1; 95% CI, 1.3–13.4).Conclusions: Given its high prevalence in Indigenous populations, the development of clinical and prevention strategies for cannabis misuse are warranted.

K S Kylie Lee BMus(Hons) · Alan R Clough PhD · Muriel J Jaragba Cert III (Mental Health) · Katherine M Conigrave FAChAM, FAFPHM · George C Patton MD, FRANZCP

Naltrexone implants have not been subject to the usual rigorous scrutiny required for new devices in Australia, but are widely used through the Special Access Scheme In this issue of the Journal, Lintzeris and colleagues report eight patients with naltrexone implants who developed serious medical complications considered to be related to the implant (→ Unplanned admissions to two Sydney public hospitals after naltrexone implants).1 Intuitively, naltrexone is an attractive treatment for opioid dependence, as it is inexpensive, long-acting and generally well tolerated, and blocks the actions of heroin when taken orally. However, empirical support for naltrexone has been unimpressive,2-4 with research showing that poor adherence to treatment limits its effectiveness. An Australian study found that, while patients who adhered to treatment did well, only 2% were still taking the drug 3 months after conventional inpatient detoxification.5 Naltrexone was registered by the Therapeutic Goods Administration (TGA) in 1998 as “an aid in the maintenance of previously opiate-dependent patients who have ceased the use of opioids”.6 However, the Pharmaceutical Benefits Advisory Committee twice rejected applications for the inclusion of naltrexone in the Pharmaceutical Benefits Scheme as a treatment for opioid dependence on the grounds of lack of evidence of efficacy. Controversy over efficacy was followed by growing doubts about naltrexone’s safety. Intermittent naltrexone consumption lowers opioid tolerance, thereby increasing the risk of heroin overdose. An Australian study found the death rate for those leaving naltrexone treatment was eight times that recorded among participants leaving treatment with agonists such as methadone or buprenorphine.7 As the weakness of the case for oral naltrexone became clearer, a range of interventions were developed to overcome the inherent problems of treatment initiation and poor adherence. The publication in 1997 of an article entitled “I woke up . . . cured of heroin” in a popular Australian magazine8 sparked intense community and political interest in the initiation of naltrexone treatment during general anaesthesia or heavy sedation, followed by oral administration. This was said to be a novel, dramatically effective treatment for heroin dependence. However, subsequent evaluation showed that these approaches increased the cost of oral naltrexone without increasing efficacy.9 More recently, depot injections10 and implants of naltrexone have become the focus of public and political hope. In this historical context, it is concerning that the recent research on naltrexone implants in Australia has not followed usual scientific processes. In particular, naltrexone implants have not been subject to the usual rigorous scrutiny required for new drug products seeking registration in this country. Nevertheless, they are available through the TGA Special Access Scheme; there is no requirement for TGA approval for access to unapproved goods in Australia for Category A patients under this Scheme, and no apparent requirement for collection of efficacy or safety data. Supporters of the naltrexone implant have argued that heroin injectors meet the criteria for Category A patients under the Scheme as “persons who are seriously ill with a condition from which death is reasonably likely to occur within a matter of months, or from which premature death is reasonably likely to occur in the absence of early treatment”.11 Most Category A patients have malignant conditions or rare life-threatening diseases. The annual mortality of heroin injectors is in the order of 1%12 — almost 15 times higher than expected for persons of the same age and sex with no history of heroin use, but hardly in the range generally considered appropriate for the Special Access Scheme. But the inclusion of naltrexone implants in the Scheme and their widespread use (reportedly by more than 1500 individuals) means the product has achieved a substantial market while not undergoing the rigorous evaluation usually applied to drugs before registration. Some of the implants used in Australia are produced locally, while others are manufactured overseas. There are doubts about the quality of manufacture, as well as deficiencies in the safety and efficacy data. As far as we are aware, no major national drug regulatory authority has licensed naltrexone implants for management of opioid misuse. However, a depot injection of naltrexone has been approved by the Food and Drug Administration in the United States, but only for alcohol, not opioid, dependence.10 Although the effectiveness, safety and cost-effectiveness of methadone and buprenorphine treatments for heroin dependence are supported by substantial and compelling evidence, a greater range of pharmacological treatments suited to the broad range of individual patients is required. A recent randomised controlled study of depot naltrexone for the treatment of opioid dependence had encouraging results.13 The strong theoretical rationale for the usefulness of naltrexone in treating heroin dependence justifies further rigorous investigations. However, the uncontrolled use of unregistered products of uncertain quality hampers the development of proper clinical trials. Since the thalidomide disaster in the 1960s, all new medications introduced into Australia have been regarded as ineffective and unsafe until proven otherwise. Constant vigilance is required to ensure that only new medications and devices of proven effectiveness and safety are permitted widespread use. The disturbing suggestions of mortality and morbidity from unregistered naltrexone implants make a strong case for an independent review to determine whether this treatment is sufficiently safe for such widespread use. This review should also assess whether the TGA Special Access Scheme has been used to circumvent the requirement for rigorous assessment of the quality, safety and efficacy of naltrexone implants. This assessment is the cornerstone of a drug regulatory system designed to protect the public from ineffective and unsafe medicines. The TGA has the power under the Therapeutic Goods Act 1989 (Cwlth) (s. 31A(2) and s. 41JD) to seek clarification of the Category A classification of patients, and should do so urgently regarding access to unapproved naltrexone products in Australia.

Alex D Wodak FRACP · Robert Ali FAChAM · David Henry FRCP(Edin) · Lloyd Sansom AO, PhD

To the Editor: According to a recent article in the Journal, the pervasive nature of under-age drinking underscores the need to develop prevention strategies to delay the onset of alcohol use and its adverse consequences.1 In the United States, school-based prevention programs have played a prominent role in the alcohol-use prevention scene. Drug Abuse Resistance Education (DARE), the most widely recognised school-based alcohol-use prevention effort, is an elementary school curriculum that focuses on the adverse effects of substances of misuse, and the development of skills to resist peer pressure to use. Despite its nationwide appeal, attempts to empirically evaluate the efficacy of DARE have failed to yield positive results.2 Subsequently, Mothers Against Drunk Driving developed a school-based alcohol-use prevention program called “Protecting You/Protecting Me” (PY/PM). PY/PM centres on instructing children about central nervous system development and the importance of protecting developing brains from substances of misuse. PY/PM appears to be effective in enhancing knowledge of alcohol toxicity and changing attitudes toward binge drinking,3 but its efficacy in decreasing alcohol use remains to be established. Although the efficacy of school-based alcohol-use prevention strategies has been the subject of controversy, such programs have proliferated. School-based multicomponent approaches have also emerged. Project Northland integrated school, neighbourhood, and family components in an effort to decrease alcohol use.4 Project Northland consisted of classroom curricula, extracurricular activities, and parental involvement. Twenty-four school districts were randomly allocated to receive some or all of the prevention package or a control. At the end of 3 years, significantly fewer students in the intervention school districts reported the onset of alcohol use than students in control districts. Efforts to disentangle the impact of its various components show differential effects. While the classroom curricula proved moderately effective, the strongest effects in decreasing drinking were seen for those who participated in the extracurricular activities and parent program components.4 The robust benefits noted from the parent program in Project Northland parallel effects of some other studies suggesting the utility of family-based approaches to alcohol-use prevention. In one study, the Iowa Strengthening Families Program significantly delayed the initiation of alcohol use.4 This program, which is geared towards optimising parenting skills, showed persistence of positive effects on alcohol outcomes 4 years after the intervention.4 These data suggest that parenting and family skills training may play a part in school-based alcohol-use prevention packages. Further evaluation of these programs in other countries is necessary, and may help to reduce the widespread adverse effects of early alcohol use among children.

Vania Modesto-Lowe · Nancy M Petry · Melissa McCartney

To the Editor: Recently, we treated a patient with fatal paramethoxyamphetamine (PMA) poisoning. We believe this is the first PMA poisoning to be reported in the Australian Capital Territory. PMA (street name, “death”) was first reported in the early 1970s during the emergence of recreational use of 3,4-methylenedioxymethamphetamine (MDMA [“ecstasy”]).1,2 Hyperthermia, coma and seizures are features of MDMA and PMA poisoning, but they are more severe with PMA ingestion; features of hypoglycaemia, hyperkalaemia and QRS interval prolongation are suggestive of PMA poisoning.3 Our patient was a 20-year-old man who was conveyed to the emergency department by ambulance after presumed MDMA ingestion. On presentation, he was unconscious (Glasgow Coma Score, 4/15) and had the following signs: temperature, 42.8°C; heart rate, 90 beats/min; QRS interval, 160 ms (reference range [RR], < 100 ms); blood pressure, 171/148 mmHg; oxygen saturation, 76% (RR, 95%–100%); and respiratory rate, 40 breaths/min. After intubation, external cardiac compressions and multiple DC shocks were required to restore circulation. The initial serum potassium level was 8.9 mmol/L (RR, 3.2–5.0 mmol/L). Hypoxaemia persisted, and a chest x-ray showed extensive bilateral airspace consolidation. The patient’s associates alleged that he habitually used equine clenbuterol and ovine androgen preparations in addition to ecstasy. The subsequent days were notable for resistant shock, rhabdomyolysis, cardiomyolysis and severe coagulopathy refractory to therapy. Oliguric renal failure necessitated extracorporeal blood purification. Hepatic failure and hypoglycaemia were pronounced. The most extreme biochemical derangements recorded in this case are listed in the Box. Five days after admission, the patient’s pupils were sluggishly reactive. Oculocephalic and oculocaloric reflexes were present but abnormal, while gag and cough reflexes were absent. A cerebral computed tomography scan showed extensive cerebral oedema. By Day 8, the patient had fixed pupils and worsening haemodynamic instability. He died 10 days after ingestion of PMA. The patient’s antemortem blood concentration of PMA was 2.3 mg/L — 2.0 mg/L above the typical fatal threshold of 0.3 mg/L previously reported.2-4 MDMA, methylenedioxyamphetamine (MDA) and methylecgonine were also detected at low levels. Since 2005, the Pharmacy Guild of Australia has instituted its “Pseudo Watch” program to reduce diversion of pseudoephedrine to illicit methamphetamine manufacture by a combination of retail restrictions and recording details of purchasers judged genuine. Supporting legislation varies by state.5 However, PMA is made from the readily available and unmonitored precursor, anethole. Further, PMA has a slower onset of action than MDMA, leading to the possibility of additional doses being ingested while awaiting effects. We believe medical practitioners should consider PMA poisoning in cases of severe reactions to ecstasy, especially those in which hypoglycaemia and hyperkalaemia are present. A “market” shift in drug use towards the more lethal PMA because of reduced availability of pseudoephedrine would be a cause for concern. Laboratory markers of multisystem organ dysfunction in a case of PMA poisoning Biochemical marker Extreme value (peak or nadir) Reference range Creatine kinase (U/L) 58 358 20–200 Troponin I (U/L) 85.83 < 0.06 Bilirubin (μmol/L) 412 2–20 ALT (U/L) 3961 < 55 Ammonia (μmol/L) 219 10–50 Platelet count (× 109/L) 18 150–400 ALT = alanine aminotransferase. PMA = paramethoxyamphetamine.

Paul G Lamberth · Geoff K A Ding · Liisa A Nurmi

Our aim was to disseminate research results about the very high rates of cannabis use in three remote Aboriginal communities in Arnhem Land, Northern Territory, to the study populations. To achieve this we translated prevalence estimates, using local concepts of life stages, numbers and quantities. The reaction of the local community to results presented in this way was characterised by the phrase used when understanding something for the first time: Wa! Ningeningma arakba akina da! (“Oh! Now I know, that’s it!”). To successfully disseminate research findings in these communities, it is critical to undertake comprehensive community liaison, to find common conceptual understandings and to build the skills of local Indigenous researchers.

K S Kylie Lee BMus(Hons) · Muriel J Jaragba Cert III(Mental Health) · Alan R Clough PhD · Katherine M Conigrave FAChAM, FAFPHM, PhD

To the Editor: In Australia, the packaging of alcoholic beverages, unlike that of non-alcoholic beverages, is not required to display a list of ingredients or nutritional information, such as the amount of sugar, calories, and any preservatives contained in the drink.1 It is possible that consumers, especially some population groups such as weight-conscious young women, might be less inclined to drink as much alcohol if they knew the calorie content of what they were consuming. There has been no published research on whether Australian consumers want this information. In April 2007, we invited (by letter and email) a random sample of 13 000 students aged 17–25 years at an Australian university to complete a web survey on alcohol consumption, health effects, and attitudes toward nutrition/ingredient labelling. Of the students invited, 7237 responded (56% response rate), and 6497 of these (90%) had consumed alcohol in the preceding 12 months. Results suggest that more than three-quarters of this population group want to see both ingredients and nutritional information displayed on alcoholic beverage packaging (Box). No more than 4% of respondents disagreed with each of these measures. Support for labelling of information among people who exceeded National Health and Medical Research Council (NHMRC) guidelines for avoiding acute harm (no more than four drinks per occasion for women; no more than six for men)2 was somewhat lower than in moderate or non-drinkers (ingredients: 75% v 86%, P < 0.001; nutritional information: 72% v 78%, P < 0.001). Support for the labelling of ingredients was somewhat greater among women than men (85% v 75%, P < 0.001), while support for the provision of nutritional information was considerably greater among women (83% v 65%, P < 0.001). We have been unable to find any studies on the effect of ingredient or nutritional information labelling on drinking behaviour. There would be value in knowing whether such labelling might influence beverage choice or overall alcohol consumption. There has been considerable debate on the effectiveness of warning labels of the type introduced in the United States in 1989, that emphasise the dangers of alcohol impairment while driving.3 A recent review of scientific studies suggested that these warning labels have no measurable effects on drinking behaviour.4 One might therefore expect there to be little or no effect of ingredient or nutrition labels. However, it is possible that the current preoccupation with weight gain in many developed countries, including Australia, might be a more compelling motive for behaviour change than alcohol-related injury risk. Regardless of whether such labels might affect drinking behaviour, it is hard to understand why alcoholic beverages are not subject to the same requirements for disclosing ingredients and nutritional information as non-alcoholic beverages. While the results of our survey cannot be extrapolated to the entire Australian population, the strength of support for (and lack of opposition to) these measures, even among heavy drinkers, suggests that bringing alcohol packaging into line with non-alcoholic beverage packaging would have public support. Responses to survey statements* Statement and response Women Men All It should be a requirement that the ingredients in alcoholic beverages are displayed on the bottle/can/cask Strongly agree 1991 (48%) 1239 (40%) 3230 (45%) Agree 1501 (36%) 1104 (36%) 2605 (36%) Neither agree nor disagree 572 (14%) 651 (21%) 1223 (17%) Disagree 49 (1%) 85 (3%) 134 (2%) Strongly disagree 5 (< 1%) 30 (1%) 35 (< 1%) Total 4118 (100%) 3109 (100%) 7227 (100%) It should be a requirement that nutritional information (eg, the amount of sugar and kilojoules) is displayed on bottles/cans/casks of alcohol Strongly agree 1890 (46%) 1016 (33%) 2906 (40%) Agree 1529 (37%) 1018 (33%) 2547 (35%) Neither agree nor disagree 607 (15%) 864 (28%) 1471 (20%) Disagree 79 (2%) 149 (5%) 228 (3%) Strongly disagree 11 (< 1%) 61 (2%) 72 (1%) Total 4116 (100%) 3108 (100%) 7224 (100%) * Not all respondents answered these questions.

Kypros Kypri · Alexandra McManus · Peter M Howat · Bruce R Maycock · Jonathan D Hallett · Tanya N Chikritzhs

Objective: To compare demographic and clinical characteristics of methamphetamine users and patients with other toxicology-related problems requiring medical intervention in a hospital emergency department (ED).Design and setting: Prospective observational study of toxicology-related presentations to the ED of St Vincent’s Hospital (SVH), Sydney, an inner-city tertiary hospital, between 1 October and 31 December 2006.Main outcome measures: Differences between methamphetamine-related and other toxicology-related presentations to the ED in relation to behaviour, mode of arrival, accompaniment, need for scheduling, location of drug use, intravenous drug use history, psychiatric history and demographic characteristics.Results: During the study period there were 10 305 patient presentations to SVH ED; 449 (4%) were toxicology-related presentations, of which 100 (1% of total) were methamphetamine-related. Methamphetamine users were significantly more agitated, violent and aggressive than patients with other toxicology-related presentations and significantly less alert, communicative and cooperative (P < 0.001); 24% of methamphetamine users (24/100) arrived with police accompaniment versus 9% of other toxicology patients (33/349) (P < 0.001). Methamphetamine users were more likely to have a history of intravenous drug use and mental health problems (P < 0.001); 39% of methamphetamine presentations (39/100) required scheduling under the Mental Health Act 1990 (NSW) compared with 19% of other toxicology-related presentations (67/349) (P < 0.001); 43% of methamphetamine-related presentations (43/100) involved drug use on the street compared with 24% of other toxicology-related presentations (83/349) (P < 0.001). Two-thirds of all methamphetamine users were male, and the most common age group for both male and female users was 26–30 years. The mean age and sex distribution of patients with other toxicology-related presentations were not significantly different. Among methamphetamine users, 27% of women (9/33) were in the 21–25-year age group compared with 10% (7/67) of men (P < 0.001).Conclusion: There were significant differences between methamphetamine-related and other toxicology-related presentations to SVH ED. Methamphetamine users were more aggressive, violent and dangerous, and thus more likely to pose a risk to health personnel and others. Methamphetamine appeared to be used consistently, rather than as an episodic “party drug”.

Philippa J Bunting BBus, CA · Gordian W O Fulde MB BS, FRACS, FACEM · S Lesley Forster MB BS, FRACMA, FAFPHM