Metabolic diseases

Objective: To investigate the relationship between a child’s weight and a broad range of family and maternal factors.Design, setting and participants: Cross-sectional data from a population-based prospective study, collected between January 2004 and December 2005, for 329 children aged 6–13 years (192 healthy weight, 97 overweight and 40 obese) and their mothers (n = 265) recruited from a paediatric hospital endocrinology department and eight randomly selected primary schools in Perth, Western Australia.Main outcome measures: Height, weight and body mass index (BMI) of children and mothers; demographic information; maternal depression, anxiety, stress and self-esteem; general family functioning; parenting style; and negative life events.Results: In a multilevel model, maternal BMI and family structure (single-parent v two-parent families) were the only significant predictors of child BMI z scores.Conclusion: Childhood obesity is not associated with adverse maternal or family characteristics such as maternal depression, negative life events, poor general family functioning or ineffective parenting style. However, having an overweight mother and a single-parent (single-mother) family increases the likelihood of a child being overweight or obese.

Lisa Y Gibson MPsych, PhD · Susan M Byrne MPsych, PhD, DPhil(Oxon) · Elizabeth A Davis MB BS, FRACP · Eve Blair BSc, PhD · Peter Jacoby BA(Hons), MSc · Stephen R Zubrick MSc, MA, PhD

Objective: To examine overweight and obesity in Australian children followed through to adulthood.Design and participants: A cohort study of 8498 children aged 7–15 years who participated in the 1985 Australian Schools Health and Fitness Survey; of these, 2208 men and 2363 women completed a follow-up questionnaire at age 24–34 years in 2001–2005.Main outcome measures: Height and weight were measured in 1985, and self-reported at follow-up. The accuracy of self-reported data was checked in 1185 participants. Overweight and obesity in childhood were defined according to international standard definitions for body mass index (BMI), and, in adulthood, as a BMI of 25–29.9 and ≥ 30 kg/m2, respectively, after correcting for self-report error.Results: In those with baseline and follow-up data, the prevalence of overweight and obesity in childhood was 8.3% and 1.5% in boys and 9.7% and 1.4% in girls, respectively. At follow-up, the prevalence was 40.1% and 13.0% in men and 19.7% and 11.7% in women. The relative risk (RR) of becoming an obese adult was significantly greater for those who had been obese as children compared with those who had been a healthy weight (RR = 4.7; 95% CI, 3.0–7.2 for boys and RR = 9.2; 95% CI, 6.9–12.3 for girls). The proportion of adult obesity attributable to childhood obesity was 6.4% in males and 12.6% in females.Conclusion: Obesity in childhood was strongly predictive of obesity in early adulthood, but most obese young adults were a healthy weight as children.

Alison J Venn BSc(Hons), PhD · Russell J Thomson BSc(Hons), PhD · Michael D Schmidt BS, MS, PhD · Verity J Cleland BAppSci(Hons) · Beverley A Curry BSc, MSc · Hanni C Gennat BSc, PhD · Terence Dwyer MB BS, MPH, MD

To the Editor: The report by See and colleagues on an accidental death from acute selenium poisoning1 draws attention to a misconception among some health-conscious consumers that, because selenium is obtainable without a prescription, it is safe to take in high doses. Selenium is available over the counter in tablets containing as much as 200 μg. The only advice printed on packs is not to exceed the recommended daily intake, which is not specified (the current Australian values are 70 μg and 60 μg per day for men and women, respectively). There is no mention of the upper limit of 400 μg, beyond which there is risk of toxicity. Selenium supplements are consumed by many people worldwide. Up to 9% of adults in the United States use these supplements.2 Consumption is much the same elsewhere in the Western world. They are used by many in the belief that their dietary intake of selenium is inadequate, and that the supplement will protect them against a variety of illnesses. Consumers get information from several sources, not least the general media and the Internet. These sources can seriously mislead, especially when they misinterpret the results of clinical trials and make exaggerated claims of health benefits. Those who rely on such popular, but simplistic, information can reach false and sometimes dangerous conclusions. Health advisors who become aware that patients are self-medicating with selenium need to point out the dangers. Unfortunately, after years of teaching students of medicine and other health-related fields about trace elements, I know that many graduates do not have enough knowledge in this area to provide accurate guidance. Even if they want to learn more by consulting current literature, the sheer volume of articles can deter them. It is for this reason that I wrote the book Selenium in food and health3 — to provide an up-to-date, scientifically based review of the nature and role of selenium in human health and metabolism. I hope that the book’s readable and user-friendly style will make it easy for overburdened professionals to learn enough about this element to help prevent the sort of tragedy described by See and colleagues.

Conor S Reilly

To the Editor: It is of great concern to me that the recent case report Accidental death from acute selenium poisoning by See and colleagues1 inappropriately cast doubts on the safety of complementary and alternative medicines (CAM). This incident should be placed in its correct context. The guidelines are clear for listed complementary medicines (ie, compounds or formulas registered and approved by the Australian Register of Therapeutic Goods for distribution in Australia).2 As a trace element, selenium is required in microgram amounts. The Therapeutic Goods Administration stringently regulates its use in nutritional supplements in Australia, with an allowed limit of 26 μg per daily dose (as selenomethionine) in unrestricted products, and 50 μg per daily dose (as selenite) in restricted, pharmacy-only supplements. This is considerably less than the “no observed adverse effects level” for selenium, which is as high as 400 μg per day,3 as noted by See and colleagues. Furthermore, even at these low doses, CAM products that contain selenium must carry substantial “red flag” label warnings. Bulk sodium selenite powder — the form which led to this fatality — is definitely not dispensed as a complementary medicine. Nevertheless, the authors of the case report conclude that “adverse outcomes of complementary and alternative medicines should be better publicised and more stringently reported to the Adverse Drug Reactions Advisory Committee (ADRAC)”. While this may be a commendable recommendation, it is inappropriate and incongruous with the findings presented in this case report. Furthermore, the sodium selenite used by nutritional doctors is administered as a liquid at a dose of 50 μg per drop, and is a restricted S4 prescription-only product. To achieve a dose of 10 g of sodium selenite, as taken by the reported patient, would require ingestion of 115 bottles of the registered S4 supplement or, even less plausibly, 400 000 doses of a listed CAM supplement. Neither of these preparations was implicated in the reported case. So why then are the authors of this case report asking for increased vigilance for complementary medicines? It is surely the interchange between the pharmacist and the customer that lies at the heart of this matter. Had a listed selenium product been dispensed, this poisoning would not have occurred.

Ian Brighthope

To the Editor: I wish to address a statement made in a recent case report in the Journal entitled Accidental death from acute selenium poisoning.1 The authors claim that the death of a 75-year-old man after ingesting 10 g of sodium selenite “exposes the myth that natural therapies are inherently safe”. The patient actually purchased sodium selenite powder and tablets. This is a restricted substance and an industrial chemical which would certainly have been labelled a poison. It should be noted that the maximum recommended daily dose of selenium in complementary medicines in Australia is 52 μg.2 The authors of the case report do point out that the patient took more than 10 000 times the recommended dose of selenium which would be available from a medicine. (My calculations put this closer to 20 000 times.) An individual drinking more than 10 000 times even the daily recommended amount of water would probably not end up in much better shape. Is this evidence of an underlying agenda to discredit natural products? The Complementary Healthcare Council of Australia recommends that consumers take steps to thoroughly inform themselves about products, preferably by asking their health care practitioner. We also urge them to inform their health care practitioner of which medicines, complementary or otherwise, they are taking. The incident involving the sodium selenite is regrettable, but for the authors to link the product and this case of fatal ingestion to exposing the myth that natural therapies are safe is, at best, ridiculous, with no foundation. They also state that adverse reactions to complementary and alternative medicines should be better publicised and more stringently reported to the Adverse Drug Reactions Advisory Committee. Adverse reactions are routinely reported and publicised for all medicines, and have been for some time, as any check of the website of the Therapeutic Goods Administration will show.3,4 I agree with the authors that the case highlights the dangers of consumers’ reliance on the Internet. Local Internet sites that advertise therapeutic goods must conform to the requirements of the Therapeutic Goods Advertising Code, as well as the Therapeutic Goods Act 1989 (Cwlth) and Regulations. However, overseas sites are not necessarily regulated or policed, and may provide inappropriate and misleading information. While our industry’s products are low risk, they should be taken, like other medicines, with due care.

Tony Lewis

In reply: The myth we referred to is the commonly held misperception by a significant percentage of the population that natural therapies are inherently safe. As Lewis and Brighthope very correctly point out, the dose ingested by our patient was hugely in excess of any recommended maximum. We believe this is evidence of the misperception, as most patients would not dream of taking 10 or 20 thousand times the maximum dose of “non-natural” remedies, because they recognise that all such remedies have side effects. Our patient’s confidence that he could safely take such a huge dose was, we consider, at least partly a consequence of his belief in the myth that natural therapies are safe. The fact that the dosage of selenium in nutritional supplements is strictly regulated does not prevent problems such as this — where patients obtain information of variable quality on the Internet, make their own arrangements to obtain the product, and then ingest a toxic amount. Our article was in no way part of “an underlying agenda to discredit natural products”; it merely highlighted the risks inherent in self-medication based on information of variable quality obtained from the Internet, coupled with the impression that natural therapies are inherently safe. We hope that our call for adverse outcomes of complementary and alternative medicines to be better publicised will go some way to preventing such a tragic error occurring again.

Peter S Lavercombe

Government, industry and the community can work together to reduce price disparities An Aboriginal Health Worker, Marinka Burton, shops at one of the Mai Wiru (good food) stores in the Pitjantjatjara Lands, South Australia. Details of the Mai Wiru program can be found at http://www.nganampahealth.com.au With the New Year come those grand statements of good intent — to eat less and live longer. But resolving to eat less is a luxury reserved for affluent people. This New Year, most of the world’s population will still be seeking to increase their food supply. This is not a matter irrelevant to Australia: Harrison and colleagues (page 9) remind us that not all Australians have an abundant, affordable and continuous supply of food.1 In their article, they report on a series of surveys — the Healthy Food Access Basket (HFAB) surveys — of selected food stores in Queensland. The surveys showed that, to meet their families’ basic food needs, Australian residents in very remote areas paid an average of about 30% ($114) more each fortnight than people living in cities. The price disparity was greater for basic, healthy food items than for “unhealthy” items such as takeaway food, soft drinks and tobacco. Moreover, at the time of the surveys, fewer of the basic healthy foods were available in remote stores than in city stores. Of particular concern were the higher increases in food prices over time in very remote areas — for example, between 2001 and 2004, the cost of the HFAB in very remote areas increased by 18% ($77.00), which was greater than the rise in the Consumer Price Index. Remote Australia is home to many Indigenous Australians. They are doubly disadvantaged, paying more for food and other essential goods, and having the lowest incomes of any population group. A detailed study of costs and incomes in a remote Indigenous community in South Australia found that basic living costs consumed up to 85% of family incomes, with food accounting for 35% of the total.2 In contrast, Australians in general spend less than 20% of the family income on food.3 Although remote Indigenous communities obtain their food from various sources, the local store remains the largest supplier of foods.4 Self-sufficiency in food (especially in the face of increasing drought) is not a viable option. Thus, inequitable food pricing is an issue for all remote communities. The poor health and nutritional status of Indigenous Australians, including extreme rates of obesity, diabetes mellitus, cardiovascular disease and end-stage renal disease, have been amply documented.5 The links between poverty, food insecurity and obesity have recently been outlined by Drewnowski and Specter,6 who argue that poor people all over the world maximise calories per dollar spent. Thus, less expensive, energy-dense foods with high fat and sugar content always win out in the shopping basket over more expensive, less energy-dense foods such as fruit and vegetables. Reducing the disparity between food prices in cities and remote areas would be one way to help Indigenous families make healthier food choices. Why are food prices higher in remote areas? Investigators have identified several reasons.7,8 Refrigerated road transport for food is expensive, and made more so by the goods and services tax (GST) and rising fuel costs. In addition, in the wet season, some communities rely on air transport for their supplies. Poor business and stock management practices, lack of accountability, and unusual or corrupt behaviour by store managers have meant higher mark-ups in stores. The lack of clear store governance roles and procedures set down by community committees has hindered attempts to improve store management practices. Store expenses, including managers’ salaries (set high to encourage recruitment to remote areas), electricity, shipping, refrigerated storage and stock spoilage costs, are often higher than those incurred by city retailers. Because of the small populations in remote areas, opportunities for achieving economies by bulk-buying from large wholesalers are limited. What is being done? An impressive array of local initiatives has been described in FoodNorth, a report commissioned by the Western Australian Government on behalf of the “Top End” states and the Northern Territory.7 The report investigated the issues of excessive food costs and limited availability, and documented examples of promising programs from remote Australia that address these problems. Recently, federal, state and territory agencies have initiated more expansive programs, including the Remote Indigenous Stores and Takeaways project and a new company, Outback Stores, established by Indigenous Business Australia with significant federal funding.9,10 These projects have been established in recognition that remote-area food stores are commercial enterprises (although in many cases community-controlled) and must make a profit to survive. At the same time, those concerned with the health and wellbeing of remote communities argue that remote stores have a social responsibility to supply healthy foods to communities that depend entirely on their stock. These dual, and potentially opposing, objectives of profit and social responsibility present a difficult, but not insurmountable, tension for food retail businesses in remote areas. Indeed, there have been considerable shifts in recent years in some communities, whose stores are pursuing better business practices for bigger profits, while improving the quality of the produce they sell — for example, by using multiple strategies that outline the roles and responsibilities of the store, the types of foods to be stocked and promoted, and the accountability requirements of managers to reduce store expenses. Improving retail management practices is expected to cut the need for high mark-ups on prices. Some communities are establishing buying groups to enable stores to bulk-buy at wholesale prices. Community stores are developing guidelines and manuals to improve training and industry practice. An example is the Freight improvement tool kit, which is designed to improve the efficiency of cold-chain perish-able food transport to remote areas.11 Schemes to recruit and train Indigenous people in retailing aim to improve the efficiency of store operations as well as providing employment opportunities. Leaders in the retail grocery industry, including Coles and Woolworths, are providing considerable pro bono support. In parallel, local communities are expanding and improving banking services to minimise stores’ financial losses from unofficial loans and credit lines. What can others do to help and support these heroic efforts? There is no shortage of ideas and plenty of work for us all — food retailers, bankers, food transport companies, land councils, Indigenous-run businesses, employment program managers, governments, health professionals, health-related data collection agencies, and academics. Public–private partnerships, particularly for retail and business training for Indigenous communities, need to be fostered and maintained. Government assistance to minimise GST costs and perhaps subsidise food transport costs is worthy of consideration. Continued support and investment in the current promising initiatives are required, including funding to evaluate programs and ensure they lead to reduced prices of healthy foods in remote areas, as well as other expected benefits such as improved employment rates, incomes and health of remote-dwelling Australians. To this end, several groups have argued for the development and maintenance of a system for routine monitoring of prices of selected foods, and a family food basket, Australia-wide.7,12,13 The HFAB surveys provide a useful model for further development of a national food price monitoring initiative. This New Year, let us resolve to help solve the problems of Australians living in remote areas who pay higher prices for food than we pay, but whose ability to pay is less than ours. Indeed, let us go beyond a resolution and — through greater citizen action, good business and a modicum of government intervention — assist our remote communities in righting this wrong.

Karen L Webb PhD, MPH · Stephen R Leeder AO, PhD, FRACP, FAFPHM

Objective: To assess changes in the cost and availability of a standard basket of healthy food items (the Healthy Food Access Basket [HFAB]) in Queensland over time.Design and participants: A series of four cross-sectional surveys (in 1998, 2000, 2001 and 2004) describing the cost and availability of foods in the HFAB over time. In the latest survey, 97 Queensland food stores across the five Australian Bureau of Statistics remoteness categories were compared.Main outcome measures: Cost comparisons for HFAB items by remoteness category for the 97 stores surveyed in 2004; changes in cost and availability of foods in the 81 stores surveyed since 2000; comparisons of food prices in the 56 stores surveyed in 1998, 2000, 2001 and 2004.Results: In 2004, the Queensland mean cost of the HFAB was $395.28 a fortnight. The cost of the HFAB was 29.6% ($113.89) higher in “very remote” areas than in “major cities” (P < 0.001). Between 2001 and 2004, the Queensland mean cost of the HFAB increased by 14.0% ($48.45), while in very remote areas the cost increased by 18.0% ($76.93) (P < 0.001). Since 2000, the annualised per cent increase in cost of the HFAB has been higher than the increase in Consumer Price Index for food in Brisbane. The cost of healthy foods has risen more than the cost of some less nutritious foods, so that the latter are now relatively more affordable.Conclusions: Consumers, particularly those in very remote locations, need to pay substantially more for basic healthy foods than they did a few years ago. Higher prices are likely to be a barrier to good health among people of low socioeconomic status and other vulnerable groups. Interventions to make basic healthy food affordable and accessible to all would help reduce the high burden of chronic disease.

Michelle S Harrison BSc, GradDipDiet, MPH · Terry Coyne BSc, MSc, PhD · Amanda J Lee BSc(Nutr), PostGradDipDiet, PhD · Dympna Leonard BSc(Diet), MPH · Simone Lowson BAppSc(Nutr), PostGradDipDiet, MPH · Anita Groos BSc(Hons), MSc, DrOecTroph · Bronwyn A Ashton BHMS(Ed), GradDipNutrDiet, MMedSc

Awareness of a serious Indigenous health problem in Australia did not emerge until the 1960s and 1970s. Much attention was focused at the time on poor pregnancy outcomes, high infant and young child mortality rates, and childhood malnutrition and impaired growth, often associated with high infectious disease burdens. Although that situation has improved somewhat, Indigenous infant and child health is still poor compared with that of other Australian children. Over recent decades, there has been a rapid rise among Indigenous people of nutrition-related “lifestyle” disorders such as obesity, cardiovascular disease, type 2 diabetes mellitus and chronic renal disease and their complications. This epidemic of disabling and often fatal chronic diseases in Indigenous Australians is also occurring in disadvantaged groups in many other countries. Control of this potentially disastrous epidemic must become a much higher priority in Indigenous health programs. Governments must commit to this task in cooperation and collaboration with Indigenous organisations and communities.

Michael S Gracey AO, MD, PhD, FRACP

To the Editor: To control the modern epidemics of preventable disease, Australia’s dietary guidelines recommend moderation in four nutritional areas — fat, saturated fat, sugar and salt. In spite of this, the obesity and diabetes epidemics seem unstoppable.1 This is hardly surprising — these guidelines seldom reach the public, and they recommend “moderation” without defining it. Zimmet and James recommend “traffic-light” food labels (red, amber, green) as a way of educating shoppers in the nutritional quality of foods.1 Traffic-light food labels2 promote the moderation message, with moderation indicated by an amber colour. Shoppers can see at a glance a food’s profile of compliance with the guidelines for each of the four areas where they call for moderation. Thus, salt content is moderate when the light for salt is amber, high when it is red and low when it is green. The same applies to fat, saturated fat and sugar. The colour coding is based on concentration in grams per 100 g or per 100 mL, with arbitrary boundaries (Box 1 and Box 2). The more green lights a food has, the healthier it is. With the aid of these labels, health professionals can treat hyperlipidaemia by dietary restriction, giving patients advice to shop exclusively for foods with green lights for fat and saturated fat. They can treat prehypertension (blood pressure, ≥ 120/80 mmHg) and thereby prevent hypertension by advising patients to eat foods with green lights for salt and green or amber in every other area.3-5 With the intention being to “guide the traffic”, the best approach would be flexible, holistic and specific for each food. For example, an amber light could recommend olive oil in moderation, even though it happens to be 100% fat. The natural sugar content of fresh fruits is high enough to give many fruits an amber rating, but moderation is hardly the right message for fruit. Australian traffic-light labels could avoid this, as the Australian dietary guidelines speak only of added sugar. Australia might add a traffic-light label for energy density (showing the same three colours based on kJ/100 g), and expand the saturated fat category to include trans fat, with very low thresholds triggering automatic red lights. Many shoppers would be surprised to find several of Australia’s best-selling breakfast cereals carrying two red lights (for added sugar and salt) and many processed meats with three or four red lights (for energy density, fat, saturated fat and/or salt). The Council of Australian Governments has announced a national campaign to arrest the growing epidemic of childhood obesity. Traffic-light labels would enable parents to protect their families from obesity by shopping almost exclusively for foods with green and amber traffic-light labels for fat, saturated fat, and added sugar. Food choices to control obesity involve a radical change in shopping behaviour, and traffic-light labels are expressly designed to promote radical change. They need to be mandatory, and they need to replace industry-sponsored schemes, which we believe are less likely to alter a customer’s buying patterns. 1 Lower and upper boundaries for the moderate (amber “traffic light”) category set in 2006 by the UK Food Standards Agency2 Food component Boundaries Fat Solids 3–20 g/100 g Drinks 1.5–10 g/100 mL Other liquids 3–20 g/100 mL Saturated fat Solids 1.5–5 g/100 g Liquids 0.75–2.5 g/100 mL Sugar Solids 5–15 g/100 g All liquids 2.5–7.5 g/100 mL Salt Solids 0.3–1.5 g/100 g All liquids 0.3–1.5 g/100 mL (equivalent to sodium 118–590 mg/100 g) The UK traffic-light label boundaries shown above treat all sodium as sodium chloride. If 118 mg is rounded to 120 mg/100 g, the boundary between moderate- and low-salt foods agrees with the international definition of low-salt foods (sodium, ≤ 120 mg/100 g). Front-of-pack traffic-light labels do not replace the technical Nutrition Information Panel. Beneficial nutrients are best promoted in this panel and, where permitted, in nutritional claims. The website <http://www.saltmatters.org> carries a longer article on the basic issues (click on Traffic Lights). 2 Example of traffic-light labelling Food carrying this label would be high in fat and saturated fat, low in sugar and medium (moderate) in salt. Red lights flag nutrient excess which is associated with preventable health problems, including, in this example, obesity, heart disease, metabolic syndrome and diabetes.

Trevor C Beard · Caryl A Nowson · Malcolm D Riley

A recent conference raised issues about the environment in which lifestyle choices are made Even before it had started, the recent 1-day conference “Obesity: should there be a law against it?” provoked controversy. The very title of the conference, convened by the University of Sydney’s Centre for Health Governance, Law and Ethics and the Australian and New Zealand Institute of Health Law and Ethics, elicited outraged responses. The recipient of much of the outrage, Conference Convener, Roger Magnusson (Associate Professor, Faculty of Law, University of Sydney), explained to the conference attendees that law’s perceived role in society is all about coercion. While law is a potent tool for public health and disease prevention, it needs to be able to “justify its involvement and defend itself from ideological attacks”. The conference’s quirky title went to the very core of the issue. Surely, adults have a right to choose to be overweight if it fits with their desired lifestyle. Shouldn’t the law stay away from our refrigerators and couches? An insightful early question from the floor was, “How can the law help frame the debate which is now framed as freedom of choice versus paternalism?” A distinguished international group of speakers presented a range of approaches to this dilemma. The Australian context: Boyd Swinburn (Chair in Population Health, School of Exercise and Nutrition Sciences, Deakin University) considered obesity in terms of the conventional epidemiological triad, where host factors (human biology and behaviour) interact with vectors (excessive energy intake and inadequate expenditure) and the environment (physical, economic, policy and sociocultural). By far the major environmental drivers, said Swinburn, are economic ones, and these are weighted on the side of obesity. Products such as energy-dense foods and cars are heavily promoted, while others such as bicycles, the exercise industry, and fruit and vegetables are not. “If you look at obesity from a libertarian perspective, it is difficult to argue for an approach that involves laws, regulations and enforceable policies; people have a right to be unhealthy if they choose to be. A protectionist approach can be used for children, whom it can be argued have a right to be healthy. However, even in adults you can justify policies such as detailed food labelling on the grounds that they will support healthy choices — making healthy choices easy choices.” While he acknowledged vast differences between the tobacco industry and the food industry, Chris Reynolds (Senior Lecturer in Law, Flinders University) pointed out the similarities in the way the two industries have marketed their products. Restrictions on marketing have had a major role in tobacco control, but so far in Australia, public policy for obesity has centred on exercise, education, and consideration of the built environment. Recent calls for controls on a range of other fronts, including food marketing, have been controversial and not supported by the federal government. While supportive of the idea of personal responsibility, Reynolds did not see this as excluding a community or collective response to public health issues. Personal choice will be influenced by the environment in which people are making that choice. “People are more likely to exercise personal responsibility if they’re not expected to swim against a current of advertising and promotion.” Elizabeth Handsley (Associate Professor, School of Law, Flinders University) is currently involved in a multinational study of the regulation of food advertising to children in Australia, the United States, Canada, the United Kingdom, Sweden and Norway. These countries vary in their regulatory structures, rules (from minimal restrictions to a complete ban), and sanctions imposed for breaches. Interesting issues raised include: who should be the regulator (industry is more efficient but government is more independent)?; to what extent should surveillance rely on public complaint versus active monitoring?; what are the relative roles of parents and society?; how should the “rules” be defined?; and, what sanctions should be imposed? The US and the UK: According to James Hodge (Associate Professor, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, USA), Americans are split between viewing obesity as a public health issue or as a personal issue, and are more likely to support interventions aimed at children. He gave a colourful account of a raft of US strategies, covering various areas of the law. These occur at every level of government, with state and even local government jurisdictions not waiting for the federal government to act. They include incentives to encourage healthier behaviour, disincentives to discourage unhealthy behaviour, litigation by injured (obese) people seeking recourse (this has generally not been successful and many states have introduced “personal responsibility” laws that prohibit it), and restriction of access to unhealthy foods (local governments achieve this via zoning laws). Robyn Martin (Professor, Public Health Law, University of Hertfordshire, UK, and Visiting Professor, Public Health Law, Chinese University of Hong Kong) pointed out that, although obesity affects many different nations, the context differs. In the UK, the context includes the political system, a culture of long working hours, class- and age-related food traditions, and even the climate! Over the past 5 years, obesity has been variously categorised in government documents as a medical problem, an economic problem, a societal problem, a public health problem and, most recently, by Prime Minister Tony Blair, as a personal problem. In a 2006 speech, he said: “Our public health problems are not, strictly speaking, public health questions at all. They are questions of individual lifestyle . . . the result of millions of individual decisions.” Even within this narrow framework, argued Martin, there is much that the government can do in the way of legal support and structures to make it easier for people to live healthily. A spurious dichotomy: Despite all the controversy, personal responsibility and the wider community response are not on opposite sides of the fence, says Chris Reynolds. “These two ideas are inextricably linked. One is necessarily supported and sustained by the other. The community must create the environment that maximises the potential for people to make healthy choices.” And Magnusson’s answer to that question from the floor about how the law can help reframe this debate? “We can turn it around and say that, if we really want to deliver on autonomy or individualism, we need to introduce legislation that allows people full freedom of choice.”

Ruth M Armstrong BMed

Objective: To ascertain whether current practice in teaching hospitals in New South Wales and the Australian Capital Territory delivers adequate dietary protein in the management of malnutrition in adults with cirrhosis, in accordance with European Society for Clinical Nutrition and Metabolism (ESPEN) guidelines for nutrition in liver disease.Study design: Cross-sectional study of dietitians using a self-administered, mail-back survey.Setting: Teaching hospitals in NSW and the ACT treating patients with cirrhosis.Participants: Dietitians seeing patients with cirrhosis in the 12 months prior to completing the survey.Main outcome measures: Current dietary protein prescription practice for patients with cirrhosis (with and without hepatic encephalopathy); use of nutritional supplements and enteral feeding for malnourished patients with cirrhosis.Results: Dietitians following the ESPEN guidelines were in the minority: 36% of the dietitians recommended an adequate protein intake for patients with hepatic encephalopathy. Sixty-four per cent of the dietitians had received referrals from the medical team requesting inappropriate protein-restricted diets for patients without hepatic encephalopathy. Seventy-eight per cent of the dietitians requested clarification of the recommended nutritional management of patients with cirrhosis.Conclusion: Many medical and dietetic staff inappropriately restrict protein intake of patients with cirrhosis.

Joanne K Heyman BSc(Hons) · Carol J Whitfield RN · Kaye E Brock PhD · Geoffrey W McCaughan MB BS, PhD · Anthony J Donaghy MB BS, PhD

Clinical record A 22-year-old male kitchen-hand presented with a 4-week history of extensive bruising and petechiae on his legs (Figure). He had no history of any medical conditions, except for several episodes of epistaxis in the past few months. He was not taking any medication, and there was no known familial bleeding tendency. On review, he had a large tense haematoma on his left leg that was restricting his mobility, and several smaller bruises in various stages of resolving, along with a palpable petechial rash on both legs (Figure inset). He was unable to recall any trauma that may have precipitated most of the bruises, but, on further questioning, believed that the rash may have been present for up to 2 years. He had no bruising elsewhere. His gums were swollen and bleeding, and oral hygiene was poor. Further examination was unremarkable. Systematic questioning revealed a long history of a poor diet comprised mainly of carbohydrates, with no vegetable or fruit intake. He smoked 10–15 cigarettes daily and episodically drank large amounts of alcohol. He lived with his girlfriend. A review of other systems showed no abnormalities. The results of initial investigations, including haemoglobin level, white cell count, and platelet count, were normal, but a blood film showed hypochromic, microcytic red cells. Liver function tests showed no abnormality; and levels of urea, electrolytes and creatinine were normal, as was prothrombin time. Activated partial thromboplastin time was increased at 39 s (reference range [RR], 26–34 s), with full correction on addition of normal plasma. Further investigations included a repeat measurement of activated partial thromboplastin time (34 s); and a test for levels of factors IX, XI and XII, which gave normal results, whereas the level of factor VIII was raised (249% [RR, 50%–150%]). A screen for lupus anticoagulant was negative, and assays for von Willebrand factor antigen and ristocetin cofactor gave normal results. The results of iron studies showed: iron, 6 μmol/L (RR, 9–27 μmol/L); transferrin, 3 g/L (RR, 2–3.6 g/L); transferrin saturation, 9% (RR, 20%–50%); and ferritin, 83 μg/L (RR, 50–150 μg/L). Finally, the level of vitamin B12 was within the normal range, serum folate level was > 45 nmol/L (RR, 12–32.7 nmol/L); and complement assays (C3, C4) gave normal results. On review 2 weeks later, a repeat blood test showed a low haemoglobin level at 72 g/L (RR, 130–185 g/L). There was no history of altered bowel habit or melaena, and the patient refused a rectal examination. Haptoglobin and lactate dehydrogenase levels were normal. Because of his iron deficiency and the possibility of significant occult blood loss, he was given a transfusion of packed red cells. The haemoglobin level remained stable after the transfusion. Further testing revealed a low level of vitamin C (3 μmol/L [RR, 26–85 μmol/L]), and he was prescribed oral vitamin C and iron supplements. Within a week, the condition of his legs was starting to improve. On review 1 month later, their appearance was almost back to normal. Patient’s left leg at presentation: extensive bruising and petechiae. Inset: perifollicular haemorrhages. Humans are one of the few mammals that cannot synthesise vitamin C (ascorbic acid). Stores are readily depleted, with studies showing clinical manifestations after about a month on a vitamin C-free diet.1 Vitamin C is absorbed by an energy-dependent, saturable transport system throughout the length of the small intestine, with any excess excreted by the kidneys. Ascorbic acid promotes the hydroxylation of proline and lysine residues in procollagen, helping to stabilise the collagen triple helix. It is the defect in collagen synthesis that produces most of the clinical manifestations. Vitamin C is particularly abundant in citrus fruit and many green vegetables. Scurvy is usually seen in mentally ill patients, people on “fad” diets, people who misuse alcohol, and, occasionally, elderly patients who live alone.2 Initial symptoms are non-specific, including weakness, anorexia, depression and lethargy. Subsequent dermatological features include broken and coiled hairs (due to abnormal keratin formation) and perifollicular haemorrhages and hyperkeratosis. Bleeding tends to be a late feature and affects spongy, friable gums as well as muscles, joints and skin. This is thought to be due to breakdown of the connective tissue within and supporting the vessel walls, rather than a platelet or clotting factor defect.3 Many patients with scurvy are anaemic, with contributing causes likely to be bleeding, altered absorption and metabolism of iron and folate,3 and other dietary deficiencies. Lessons from practice Scurvy can occur in apparently well-nourished populations, as a result of severely restricted food choices (eg, avoiding fruit and vegetables). It may be associated with other vitamin and mineral deficiencies. Bleeding is a late manifestation of scurvy. Our patient is interesting in that he does not seem to fit into the usual groups with a tendency to develop vitamin C deficiency. A full dietary history revealed a diet entirely comprised of Vegemite spread, cheese, bread, dry biscuits, chocolate and a cola drink, with no fruit or vegetables. The patient conceded that he had not tried any new foods for over 10 years, and, despite the recent diagnosis, was reluctant to initiate dietary change. Although such a limited food intake is probably uncommon, recent trends towards consumption of pre-prepared carbohydrate-rich food mean that scurvy or subclinical vitamin C deficiency and other vitamin and trace metal deficiencies should not be forgotten.

Sally J Mapp MB BS, FRACP, FRCPA · Paul B Coughlin FRACP, PhD

To the Editor: Tan et al1 found that patients value key elements of successful weight management, including advice on healthy eating and exercise and regular follow-up. Accredited practising dietitians (APDs) provide all of these things and have the qualifications, skills and time to work with people to effectively manage weight. APDs use the Obesity Best Practice Guidelines of the Dietitians Association of Australia, providing evidence-based dietary therapy. By working alongside general practitioners to provide individual advice, APDs ensure the best outcomes for patients. A considerable number of patients surveyed said that referral to a dietitian would be useful and that they would be likely to follow their GP’s advice if referral was recommended. The weight management roles of GPs and APDs are complementary and, by addressing any patient concerns and providing a referral to an APD, GPs can help their patients achieve their weight management goals.

Claire Hewat

Many disparate groups in Australia now concur about the need for continuous food and nutrition monitoring Poor nutrition contributes to Australia’s current health problems in several ways. Heart disease and cancer, both strongly related to nutrition, remain the leading causes of death. At the same time, the prevalence of obesity and diabetes is alarmingly high, and deficiencies of vitamin D, iodine, and calcium are re-emerging. As a consequence, policymakers, food regulators and health professionals need up-to-date and specific information about what people are eating and how much they are eating. They need to know the health and nutritional status of the Australian population. They also need to know how supplies of food and food consumption patterns are changing over time, and what food products contain. In turn, consumer education policies and tools, such as population dietary guidelines and food selection guides, need to be built on a solid foundation of knowledge about the national nutrition profile to reduce the risk of serious nutrition-related diseases and conditions. Food safety regulators also need this information to estimate current exposure to bioactive compounds that may be of concern, such as food additives and contaminants, to inform food fortification policies, and to ensure that nutrition information on food labels is relevant to current consumption patterns. Yet, Australia is unusual among its peers for not having continuous nutrition intelligence. Health-related data about Australians are compiled biannually, but current information about food and nutrient consumption, and trends in these, is conspicuous by its absence.1 The United States, the United Kingdom, and many European nations have had ongoing, systematic programs for monitoring the diet and nutritional status of their populations for many years.2-4 These programs are not confined to large countries with big budgets. For example, in 2001, New Zealand embarked on a 10-year strategic plan for a coordinated national population survey program that includes nutrition surveys in adults and another in children every 10 years, with the next surveys of adults and of children due in 2007–08, and 2012, respectively.5 In contrast, Australia has conducted only three national surveys of diet in the past 50 years: a national dietary survey of adults in 1983, and of children in 1985, and the National Nutrition Survey in 1995, which included both adults and children.6-8 Each cross-sectional survey was conducted by a different agency, using different sampling and collection methods and food composition data. These differences limit our ability to describe trends in food and nutrient consumption.9 Several state and territory governments in Australia have established monitoring systems that survey health behaviours, including food habits.10 These systems provide important information for tracking change, but food production, retailing and consumption are not limited by state boundaries, and information about selected food habits is not a sufficient base on which to build nutrition and food regulatory policy. Those with commercial as well as health interests in nutrition surveillance now favour a new national effort — one that goes beyond the brief encounters of cross-sectional surveys — to provide continuous detailed information on trends in food and nutrient consumption, the food supply and the nutritional status of Australians. Continuous nutritional surveillance must form part of a comprehensive policy to combat nutritional disorders. Where such surveillance exists, such as in the US, the data have been used to evaluate dietary guidelines, revise food selection guides,11 develop and evaluate fortification programs, set “real-life” serving sizes for nutrition information panels on food labels, make decisions about specific food processing regulations, and model the impacts of bioterrorism threats from food contamination.2 The centrepiece of the US system is the continuing National Health and Nutrition Examination Survey (NHANES), which is supplemented by many other sources of data.12 International experience suggests that there are two important actions for Australia to take in developing a food and nutrition monitoring system: 1. Establish a small, affordable, but statistically robust ongoing nutrition survey program, with data collected from a sample each year and reported cumulatively over a number of years. This program should be based within a federal agency that has health information responsibilities, uses consistent methods, can document and maintain databases, and reports on a predictable and timely basis. 2. Create a small nutrition monitoring unit to compile, disseminate and promote the use of all appropriate information about the food and nutrition situation in Australia for various policy, program, and regulatory purposes. The Australian Government Department of Health and Ageing recently commissioned the preparation of a business case for a no-frills national nutrition surveillance system in Australia, and consulted widely with stakeholders on its importance and suitability.13 Many disparate groups in Australia — in food production, marketing, regulation, and consumer health — now concur about the need for continuous food and nutrition monitoring, as well as the imperative to find workable solutions to long-term funding needs. While a national cross-sectional nutrition survey of children is currently being planned, its value would be greater if it were the start of a continuing surveillance program. In this regard, the recent announcement by the Minister for Health and Ageing of $3 million initially for a survey of diet, physical activity, and the weight status of Australian children, and $1 million annually thereafter for the collection of similar data on all population groups in Australia, is welcome, especially if it evokes a matching response from other key data users, including the states and territories.14 This may be the politically propitious moment for a long-term commitment to a system of continuous monitoring of food and nutrition in Australia.

Karen L Webb PhD, MPH · Ingrid H Rutishauser MSc · Geoffrey C Marks PhD, MS, DipNutrDiet · Gregory Masters MSc · Stephen R Leeder PhD, FRACP

To the Editor: Trans fats are produced by partial hydrogenation of liquid vegetable oils to produce oils which are more solid at room temperature and have better physical properties for food processing, such as increased shelf-life. Trans fats represent a major dietary cardiovascular disease risk, with as little as 5 g daily increasing the risk of ischaemic heart disease by 25%.1 A recently published survey of the trans-fat content of French fries and chicken nuggets purchased from two international fast food chains in 20 countries emphasises the wide variability of trans fats in different countries.2 This work highlights the potential health risks imposed by the industrially generated trans fats in these food products. Of the sampled French fries and nuggets, 20 of 39 samples from 19 different countries yielded trans-fat levels in excess of 5 g for an average serve. Interestingly, the report included no data from Australia. We have evidence that similar fast foods have substantial quantities of trans fats (putting Australia in the mid-range of the league table). The only available published results are those reported by the Australian Consumers Association (ACA) in 2005.3 The ACA tested 55 foods and found 18 had trans-fat levels greater than 2% of total fat. The interesting issue is that the ACA data show a variation in trans-fat levels of greater than 22-fold (0.8%–22.5% of total fat) in popular fast foods. Data on trans-fat levels should be available on all foods in this country, whether sold in supermarkets or to the food service industry. However, at present, there is no requirement to include trans-fat content on nutrient information panels, except when the manufacturer wishes to make a nutritional claim about cholesterol, saturated, unsaturated or trans-fatty acids.4 Many countries, including the United States, Canada and some European countries, have either placed limits on the permissions for trans fat in processed foods, or, more commonly, mandated labelling requirements. The most notable is Denmark, where legislation restricts maximal industrially produced trans fats to less than 2%.5 Not surprisingly, that country reported markedly lower trans-fat contents in fries and nuggets than those sold in Australia.2 Despite review of the “Australia New Zealand Food Standards Code”, labelling of the trans-fat content of food has not been mandated,4 and consumers and health professionals wishing to reduce their trans-fats intake remain unable to make informed choices.

David Cameron-Smith · Andrew J Sinclair

Health benefits of herbs and spices: the past, the present, the future

Linda C Tapsell PhD, MHPEd, DipNutrDiet, FDAA · Ian Hemphill · Lynne Cobiac PhD, MBA(Advanced), PostGradDipNutrDiet · David R Sullivan FRACP, FRCPA, FCANZ · Michael Fenech PhD · Craig S Patch PhD, MBA, GradDipNutrDiet · Steven Roodenrys PhD · Jennifer B Keogh MSc, DipDiet · Peter M Clifton PhD, FRACP · Peter G Williams PhD, MHP, DipNutrDiet · Virginia A Fazio MBA, MSc, GradDipDiet · Karen E Inge BSc, DipDiet

The fortification of staple foods has eliminated many deficiency diseases. Despite this, “tampering” with people’s food always provokes opposition, much of it from health professionals. Opposition is often based on self-interest, tunnel vision and theory rather than research. A historical perspective of the patterns of objections to fortification and its outcomes may help resolve the anxieties and opposing ethical positions of advocates and opponents of fortification.

Max Kamien FRACP, FRACGP, FACRRM

To the Editor: I would like to clarify several issues relating to the competing interests statement for my editorial in the 16 January issue of the Journal.1 In my statement, I declared that I have used several meal replacement products in clinical settings and that I am not employed by, and do not receive benefit from, any companies producing these products. By way of further information, I have used Optifast (Novartis) and Dr MacLeod’s (Orfam) products in clinical work in the past. These were always sold at cost to patients, or patients were referred to a chemist, so there was no direct financial benefit to me. I currently use KicStart (Pharmacy Health Solutions) as part of the kit for “Professor Trim’s weight loss program for men”. I purchase these in bulk at wholesale prices from the manufacturer and include them as part of the total program (which is much more than just meal replacement).

Garry J Egger

There is much to be gained by reducing children’s intake of soft drinks and little — except excess weight — to be lost Childhood obesity is a major health issue in Australia. In recent months, a number of organisations, including the Australian Medical Association,1 have released statements demanding stronger action on this issue, including a call to restrict access to and marketing of soft drinks to help reduce children’s consumption. However, the soft-drink industry rejects these proposals and argues that their product is being unfairly singled out for action. Further, many parents are confused as to why a drink they often consider to be a harmless treat should be labelled so damaging to their children’s health. In considering the suggested policy changes, it is therefore important to weigh up the information we currently have about the extent of soft-drink consumption, its impact on childhood obesity, and the potential of a reduction in consumption to contribute to improved weight control. The term “soft drink” covers a number of different beverages, but in Australia it is generally used to refer to carbonated beverages, and more specifically sugar-sweetened carbonated beverages. It may be assumed that other sugar-sweetened beverages, such as cordials and sweetened fruit drinks, which are consumed more regularly by young children, would have a similar impact on energy and nutrient intake. However, sugar-sweetened carbonated beverages and electrolyte drinks are usually singled out for specific attention because they are well identified products, which are readily available, marketed aggressively to teenagers, and make the largest overall contribution to the beverage intake of children. While it is widely reported that children consume too much soft drink, lack of continuous nutrition monitoring makes it difficult to provide accurate current data. Information on soft-drink consumption is available from a variety of sources using different dietary assessment methods and thus needs to be interpreted in different ways. However, the various sources of data are reasonably consistent in relation to the quantity of soft drinks consumed. A recent phone survey by Food Standards Australia and New Zealand found that 78% of all 12–17 year olds had consumed soft drink in the previous week,2 while the 1995 National Nutrition Survey found that around half of all teenagers and a surprising 26% of 2–3 year olds had consumed soft drink during the previous 24 hours. Boys tended to consume more soft drink than girls, with boys aged 16–18 years drinking an average of 480 mL each day (or 836 mL per day among those who consumed soft drink), double the consumption of girls of that age (unpublished data from the 1995 National Nutrition Survey recalculated by us to include soft drinks only. Complete data in National Nutrition Survey: foods eaten, Australia, 19953). This was equivalent to 5.5% of the average total energy consumed by 16–18 year olds or 10.8% of the energy intake of the consumers. Apparent consumption data from the Australian Bureau of Statistics, as well as industry data, suggest that the intake of soft drinks in Australia has grown rapidly in the past 30 years from around 47.3 L per person per year in 1969 to 113 L per person (children and adults) in 1999.4 While this is some way below the per capita consumption of 200 L per year in the United States, it does put Australia within the top 10 countries for consumption and represents a market of around $1.6 billion per year.5 There is reasonable evidence that a high intake of soft drinks is associated with a greater risk of weight gain and obesity. A number of US studies show a strong cross-sectional association between soft-drink consumption and excess energy intake in adolescence,6,7 and NZ children who drank soft drinks more than once a day also were found to have a significantly higher mean body mass index (BMI) than children drinking soft drinks less than once a week, even after controlling for other known risk factors for weight gain.8 Longitudinal studies provide stronger evidence of a role for soft drinks in weight gain in children, with a large observational study of 10 000 children showing a consistent relationship between consumption of sugar-added beverages and weight gain over a 2-year period.7 A smaller 19-month study of 548 children aged 11 years found that both initial consumption and increases in intake levels of soft drink were associated with increased BMI and risk of obesity.9 A 10-week feeding trial found that when overweight adults were given a supplement of sucrose, mostly in the form of soft drink, they gained on average 1.6 kg, while a control group fed an artificially sweetened supplement lost 1.0 kg.10 The low satiating properties of energy-rich fluids compared with solids has been proposed as a possible reason for the close association between energy from soft drinks and weight status.11 Only a few studies have examined the effect on weight status of interventions aimed at reducing energy intake from sugar-sweetened soft drinks. These studies support the potential of such action, while leaving many questions unanswered about how best to achieve the desired outcomes. A school-based intervention that encouraged children (7–11 years old) to reduce their intake of “fizzy” drinks was able to achieve within 1 year a significant reduction in overweight and obesity in the intervention group compared with the control group, although the design and statistical analysis of this study have been criticised. The evidence linking soft-drink consumption to weight gain and obesity, while not complete, is consistent and strong enough to support action. Soft drinks are consumed in large amounts by young people in Australia and thus the calls for curbing intake appear to be justified. As soft drinks have been linked to other health concerns such as dental disease and, moreover, provide no valuable nutrition (apart from fluids), there is potentially much to be gained by reducing the intake of these (and other) sugar-sweetened beverages by Australian children and little (except excess weight) to be lost.

Timothy P Gill PhD GradDipDiet · Anna M Rangan PhD, GradDipNutrDiet · Karen L Webb MPH, PhD

Mu Li,* Kay V Waite,† Gary Ma,‡ Creswell J Eastman§ * Senior Lecturer, School of Public Health, University of Sydney, Sydney, NSW 2006; † Technical Officer, ‡ Principal Scientist, § Director, Australian Centre for Control of Iodine Deficiency Disorders, ICPMR, Westmead Hospital, Sydney. muliAThealth.usyd.edu.au To the Editor: Iodine is essential for production of thyroid hormone. The recommended daily intake is 100 μg for children, 150 μg for adults and 250 μg for pregnant and lactating women.1 Sporadic surveys of population iodine intake in Sydney, New South Wales, between 1985 and 1992 showed median levels of urinary iodine excretion (UIE) > 200 μg/L, indicating iodine sufficiency.2 However, a recent national study demonstrated mild iodine deficiency (median UIE < 100 μg/L) in New South Wales and Victoria, borderline levels in South Australia and adequate intake in Queensland and Western Australia.3 The major sources of dietary iodine are dairy milk and dairy products, seafood and iodised salt. In Australia, few people purchase iodised salt, and, except in Tasmania, the food industry does not use iodised salt in the production and preparation of food.4 For decades, milk contaminated with iodine residues from sanitising solutions (iodophors) used in the dairy industry has probably been the largest source of iodine in the Australian diet. We undertook a survey of the iodine content of milk samples from supermarkets around metropolitan Sydney in 2001 and 2004. In each year, iodine levels were measured in 13 samples, comprising a range of milk types (including whole, full cream, lite and skim) and brands (including Dairy Farmers, Devondale, Farmdale, Farmland, Perfection, Pura and Woolworths). Iodine concentrations were highly variable. Median concentrations were 140 μg/L in 2001 (range, 60–220 μg/L) and 195 μg/L in 2004 (range, 66–412 μg/L). Iodine concentrations varied between samples of the same brand and type by up to 100 μg/L. Many samples contained less than 200 μg/L (10/13 in 2001 and 7/13 in 2004). A 1975 survey of iodine concentration in milk conducted by the Australian Consumers’ Association found mean concentrations of 593.5 μg/L and 583 μg/L in NSW and Victoria, respectively.5 Because of concerns about iodine toxicity, Food Standards Australia and New Zealand specified an iodine limit of 500 μg/L in the Food Standards Code 1982. The replacement of iodophors by other sanitisers in the dairy industry appears to be the reason for the decrease in iodine content of Sydney milk. The perception that milk is a rich source of iodine is no longer true. A cup (250 mL) of milk a day would provide at most 50–60 μg iodine, approximating a third of the daily requirement for an adult. We suggest that the reduced amount of iodine in milk is likely to be one of the explanations for the re-emergence of iodine deficiency in Sydney and perhaps elsewhere in Australia. Despite these changes, dairy milk remains an important source of dietary iodine. The iodine content in milk should be monitored.

Mu Li · Kay V Waite · Gary Ma · Creswell J Eastman

Clinical trials show partial meal replacement products to be safe, acceptable and effective when used as part of an overall low-energy diet Overweight (body mass index [BMI] > 25 kg/m2) and obesity (BMI > 30 kg/m2) are now major health concerns, being causally related to a number of metabolic disorders, and affecting at least one in two adult Australians.1 However, the long-term evidence on treatment of these conditions is disappointing. A strategy recommended in the recent clinical guidelines from the National Health and Medical Research Council is the use of low-energy meal replacement products.1 These have been marketed for many years, but have only recently been considered seriously in large clinical trials. If effective, this strategy offers promise as: it provides a discrete option for doctors dealing with a difficult condition; it is easy to administer and supervise; and it is relatively cheap. However, questions remain about the long-term outcomes and safety of meal replacement products, their effects in comparison with other strategies, and their acceptability to patients. What are meal replacements? Meal replacements are defined as “a single food or pre-packaged selection of foods that is sold as a replacement for one or more of the daily meals, but not as a total diet replacement”2 (Box 1). These replacements exert their effect through reducing portion size, and consequently energy intake.3 In patients with morbid obesity requiring large weight losses (BMI > 40 kg/m2), specially formulated very low calorie diet (VLCD) forms of meal replacement may be used in place of all meals. However, more commonly, partial meal replacements are used for one or two meals a day, with at least one usual meal consumed as part of an overall low energy diet. Here, I focus on the use of partial meal replacements, because of their wider potential clinical use. Why are partial meal replacements returning to favour? Traditionally, there has been concern about the use of any meal replacements, probably based on concerns about: the nutritional balance of some commercial mixes; potential “bounce back” weight gain on discontinuing use, when this use is unsupervised (as for any low-energy diet plan); and the fact that they may not teach users good long-term eating habits. These concerns have now been largely overcome by: advances in food technology, which allow more complete and better balanced nutrient mixes; a move towards better training of clinicians about weight control; and the fact that most reputable products are now part of a broader weight loss program, with accompanying nutritional education about non-replacement meals (Box 2). While different forms of meal replacements have been used for weight loss over many years, controlled research on the effectiveness of partial meal replacements is relatively recent. Several studies, reviews and meta-analyses now attest to the benefits of partial meal replacements. Their use commonly results in weight loss of around 9%–10% of total body weight in the short term (6–12 months), and 6%–8% in the long term (eg, 1–5 years), with no reported adverse effects when used as part of an overall low-energy diet plan.3-6 This compares favourably with a 3%–7% loss on some other types of diet plans,3-6 although at least one study showed similar short-term weight losses from meal replacements and a prescriptive, structured low-fat diet plan.7 The benefits of partial meal replacements are even more obvious when compared with no treatment. In a 5-year study, an average weight gain of over 1 kg per year occurred in control subjects, compared with a loss of 5.8 kg in men and 4.2 kg in women using partial meal replacements.8 It has been suggested that replacing two meals a day, while maintaining one other main meal, is most effective for initial weight loss, while replacing one meal a day (preferably a meal which is usually high energy, such as lunch or dinner) is enough for long-term maintenance.6 Quick effects from supervised short-term use might be expected to have the added benefit of increasing motivation for long-term lifestyle change. Several studies have also shown improvements in metabolic risk factors with use of partial meal replacement products, exceeding the changes achieved by dietary change alone (even structured low-energy diets).6,8 Partial meal replacements have particular benefits for patients with diabetes.9,10 The effects on glucose control occur within days, and last for as long as weight loss is maintained, enabling a reduction in diabetic medications, but there are also improvements in blood pressure, and serum cholesterol and triglyceride levels (probably more due to the weight loss than the meal replacement per se). Partial meal replacements appear to have an effect across a range of ages and in both sexes (although men generally have better results than women).8,11 They can be used with minimal supervision,11 but are probably most effective when closely supervised with regular follow-up.12 Most studies show greater patient satisfaction and lower drop-out rates with partial meal replacements than with other diets, possibly because use of meal replacements results in less hunger.13 Partial meal replacements also seem effective in people from low socioeconomic backgrounds,14 who are currently more likely to be overweight, and hence in greater need of weight loss treatments.1 Importantly, partial meal replacements are generally cheaper than other diet plans (Box 2), and certainly more so than non-diet meals. Meal replacements are not contraindicated in common weight-related diseases (eg, diabetes and heart disease), but food sensitivities, such as lactose intolerance or food allergies, need to be taken into account when choosing specific products. Which product should I recommend? Selection of a commercial meal replacement product in Australia is complicated by the food standards, product marketing, the different conditions under which the products can be mixed (eg, with milk or water), and confusion with VLCD foods, which are based on total meal replacements, and for which only draft standards exist. There are currently few products that satisfy all requirements for a meal replacement, although some are still promoted as such. For example, low-energy “weight loss” drinks and other (usually supermarket-supplied) products are sometimes labelled to imply they can be used as a meal replacement, despite not meeting minimum Food Standards Australia New Zealand (FSANZ) requirements (Box 1). Box 2 shows a cross section of popular products from different outlets in Australia that meet or approach the minimum standard for nutritionally balanced meal replacements. Partial meal replacements seem to be safe, acceptable to patients, and more effective over the long-term than most other diet-based weight loss techniques, although it is likely that best results will be achieved with the supervision of a clinician skilled in weight control.11 Because most individuals in modern societies consume too much energy in relation to expenditure, there now seems little reason not to prescribe properly constituted partial meal replacements for overweight patients for whom this treatment is appropriate, in line with the emerging realisation that one treatment does not necessarily fit all.15 In fact, with the trend to modern sedentary lifestyles and escalating levels of obesity, it is not difficult to imagine much of our population needing to use partial meal replacements judiciously at some time in the future for prevention or treatment of overweight and obesity. 1 Food Standards Australia and New Zealand requirements for commercial meal replacements2 Meal replacements (minimum requirements per meal) 12 g protein 850 kJ 25% of the recommended daily intake of 16 prescribed vitamins and minerals Very low calorie diets (VLCDs) (draft requirements) 1.7–3.3 MJ per day Omega-3 and omega-6 fatty acids 50 g carbohydrate per day 50 g protein per day Minimum and maximum levels for 24 prescribed vitamin and minerals 2 Characteristics of some examples of commercially available meal replacement products in Australia* KicStart VLCD (Pharmacy Health Solutions) Optifast VLCD (Novartis) Dr MacLeod’s (Orfam) Ultra Slim (Associated British Foods) Availability Pharmacies Pharmacies Doctors, clinics Supermarkets Presentation 24-sachet box 21-sachet box Single sachets Tin of powder Price per meal to patient $2.04 $2.33 $2.65 $1.00 Protein per serve† (g) 17.9 17.3 15.2 4 Carbohydrate per serve† (g) 9.8 15 19.2 20.5 Fat per serve† (g) 3.0 2.3 1.8 2.6 Omega-3 and -6 fatty acids Yes Not listed Not listed Not listed No. of vitamins and minerals 26 27 16 24 Fibre Yes Not listed Not listed Yes Total energy of prepared drink (kJ) 584 (water), 883 (skim milk) 638 (water) 640 (water) 875 (skim milk) Accompanying material on weight loss Yes Yes Yes No Qualifies as VLCD Yes Yes No No * Characteristics apply to the chocolate variety of each product. † Protein, carbohydrate and fat levels are for the dry powder. If directions are to mix with skim milk, levels of protein increase by approximately 7 g, carbohydrate by 10 g and fat by 0.2 g.

Garry Egger BA, MPH, PhD

Objectives: To examine whether children’s television viewing may be a useful indicator of risk of obesity-promoting versus healthy eating behaviours, low-level physical activity (PA) and overweight or obesity among children of primary school entry and exit ages.Design: Cross-sectional study, stratified by area-level socioeconomic status.Participants and setting: 1560 children (613 aged 5–6 years [50% boys], and 947 aged 10–12 years [46% boys]) from 24 primary schools in Melbourne, Australia, randomly selected proportionate to school size between 1 November 2002 and 30 December 2003 .Main outcome measures: Parents’ reports of the time their child spends watching television, their participation in organised physical activities (PA), and their food intake; each child’s measured height and weight and their PA levels as assessed by accelerometry for one week.Results: After adjusting for the age and sex of child, the parents’ level of education, clustering by school, and all other health behaviour variables, children who watched television for > 2 h/day were significantly more likely than children who watched television for ≤ 2 h/day to: to have one or more serves/day of high energy drinks (adjusted odds ratio [AOR], 2.31; 95% CI, 1.61–3.32), and to have one or more serves/day of savoury snacks (AOR, 1.50; 95% CI, 1.04–2.17). They were also less likely to have two or more serves/day of fruit (AOR, 0.58; 95% CI, 0.46–0.74), or to participate in any organised PA (AOR, 0.52; 95% CI, 0.34–0.80).Conclusions: Health practitioners in the primary care setting may find that asking whether a child watches television for more than 2 hours daily can be a useful indicator of a child’s risk of poor diet and low physical activity level.

Jo Salmon PhD · Karen J Campbell MPH, PhD · David A Crawford PhD

Many claims about nutrition and weight loss stem from small, short-term studies, incorrect interpretations or distortions of evidence. Our knowledge of what people eat is poor; difficulties include accurate assessment of consumption, the complex composition of foods and individual variations in nutrient bioavailability. When advice appears to be ineffective, poor compliance is a likely explanation. There is no simple solution to obesity, and no fast way to create the energy deficit required for sustainable loss of fat — weight loss requires long-term commitment to permanently change eating and exercise habits. Valid advice is to reduce overall energy intake, include more vegetables, fruits and wholegrain products and fewer foods high in saturated fat, sugar and salt. While mindful of the need to encourage individuals to make changes, the medical profession needs to lead the charge to advocate for changes to our obesogenic environment.

Rosemary A Stanton OAM, PhD

During the Australasian Antarctic Expedition of 1911–1914, Douglas Mawson and two companions, Belgrave Ninnis and Xavier Mertz, undertook an ill-fated mapping journey. Ninnis died when he fell down a crevasse, together with the sledge carrying most of their food supplies, and later Mertz became ill and died. Only Mawson returned. In 1969, Cleland and Southcott proposed that Mertz died of vitamin A toxicity and Mawson suffered from the effects of hypervitaminosis A because, with little food left, they were forced to eat their surviving dogs, including the liver. This hypothesis was supported by Shearman in 1978. After re-evaluating this hypothesis, I propose that Mawson and Mertz suffered from the effects of severe food deprivation, not from hypervitaminosis A, and that Mertz died as he was unable to tolerate the change from his usual vegetarian diet to a diet of mainly dog meat. I also suggest that Mertz’s condition was aggravated by the psychological stress of being forced to eat the dogs he had cared for for 18 months.

Denise Carrington-Smith BA(Psych), MSocSc(Archaeology)