Metabolic diseases

To the Editor: There is an established link between salt intake and blood pressure. The public health impact of a 1–3 mmHg reduction in blood pressure by lowering salt intake could be substantial. An American study found that a projected reduction in diastolic blood pressure of 2 mmHg would result in a 17% decrease in the prevalence of hypertension, a 6% reduction in the risk of coronary artery disease events, and a 15% reduction in risk of stroke and transient ischaemic attacks.1 In Finland, a one-third decrease in average salt intake achieved over 30 years was accompanied by a fall of more than 10 mmHg in the population averages of systolic and diastolic blood pressure.2 However, in the absence of active measures to reduce salt in the food supply, public health messages to reduce salt intake have largely been unsuccessful. The National Health and Medical Research Council (NHMRC) has recently revised its recommendations and now states that an adequate sodium intake for adults is 460–920 mg/day (20–40 mmol/day), with a suggested dietary target for chronic disease prevention of 1600 mg/day (70 mmol/day).3 The most recent Australian sodium intake data are from the 1995 Hobart Salt Study, in which the then national target of 6 g/day was achieved by only 6% of men and 36% of women, with an average salt intake of 7–10 g/day.4 Volunteers in weight-loss studies at the Commonwealth Scientific and Industrial Research Organisation (CSIRO) Human Nutrition unit over the past 5 years continue to have a high salt intake of 8–11 g/day (urinary sodium/24 h: men [n = 85], 181 ± 95 mmol; women [n = 189], 136 ± 61 mmol; reference range, 40–100 mmol).5 Recent data from another Australian study report similar urinary sodium concentrations.6 The average salt intake of Australian adults appears to be 7–12 g/day, which is little changed from 10 years ago. Achieving a low salt intake in the present food supply is difficult, as more than 80% of intake is from salt added to food during processing. As well as the more obvious foods in which salt is a preservative, staple foods such as bread also contain salt. The variety of foods has increased considerably, and many of the numerous processed foods now available contain very high salt levels. Processed and convenience foods frequently have salt added that the consumer cannot avoid. It is clear that large changes to the food supply are needed to reduce salt intake. We believe that salt reduction in the food supply should be the first line of attack to reduce the risk of cardiovascular disease in the population.

Jennifer B Keogh · Peter M Clifton

To the Editor: During the recent international cricket series between Australia and India, we were alarmed by the sight of our Australian cricketers prominently badged with the logo of the fast food giant KFC. Australia is experiencing an epidemic of overweight and obesity, a problem that is especially affecting children, adolescents and young adults.1 This epidemic is worsening as a direct result of unhealthy eating habits and low levels of physical activity. Obesity is associated with chronic and costly diseases that lead to premature death and ill health. These include diabetes, cardiovascular disease, respiratory problems, sleep apnoea, certain cancers, mental illness and osteoarthritis, which can begin in adolescence.1 Cricket in Australia enjoys considerable popularity and a strong national following. Our cricketers are national sporting heroes who enjoy widespread support and respect throughout the community, particularly among younger members of the community, who aspire to emulate them. Against this background, we are increasingly concerned and disappointed that Cricket Australia has a sponsorship agreement with, and consequently promotes, KFC — going as far as publicly declaring the company the “official fast food restaurant of Cricket Australia”.2 This advertising uses the standing of cricket and its players to endorse and promote unhealthy eating habits, one of the major root causes of obesity in Australia. KFC products have caloric and fat contents well above the national dietary guidelines, which recommend < 30% energy from total fat and < 10% energy from saturated fat.3 For example, a standard serve of original-recipe chicken contains about 58% total fat and 24% saturated fat.3 Furthermore, we have shown that even one common KFC meal per week can adversely affect recommended healthy diets.4 It is ironic and regrettable that Cricket Australia, while having done so much for the sport, encourages the promotion of unhealthy, high-fat, high-calorie KFC products that negate the benefit of increased physical activity associated with playing cricket. With the explosion of obesity-related illness, we need champions to encourage health-promoting behaviours, particularly healthy eating and increased physical activity. The enthusiastic encouragement of unhealthy and undesirable eating habits should have no place in sporting sponsorship. Not so long ago, similar sentiments were being expressed about tobacco sponsorship of sport, which fortunately has been eradicated. Cricket Australia should consider its responsibilities to Australia’s children and youth and review its sponsorship by KFC. This would benefit the health of the community and demonstrate leadership and social responsibility by Cricket Australia and Australia’s elite cricketers.

Stephen Colagiuri · Ian D Caterson

In reply: Cricket Australia (CA) actively supports physical activity, healthy eating and healthy lifestyles and continues to invest considerable effort in encouraging Australians to play cricket, in everything from formal, organised competitions to social games in the backyard, in parks and schoolyards and at the beach. In a time of declining community physical activity, we are heartened to see that active participation in cricket is growing strongly, and note that female cricket is the fastest growing female sport in Australia. As a community-based, not-for-profit organisation, we are heavily dependent on the support of all of our sponsors, including KFC, to be able to implement the activities we undertake. These range from community-based programs that get kids running around outside to programs in schools, clubs and Indigenous communities, and further activity needed to develop and put elite international cricketers onto the field. In relation to KFC, we believe in a little of everything and everything in moderation. Setting aside the truly elite athletes, the formula that is going to work best for most cricketers and cricket fans is reasonable, not extreme, training and physical activity, together with a balanced diet, not one that features total abstinence from high-energy foods. Our view on alcohol is the same. Our CA advertising featuring Merv Hughes encourages fans to enjoy a beer, but not at the rate of one per over. The overall issue is about balance. Consumer research — commercially confidential, so it can’t be referenced here — shows that KFC consumption in Australia is an occasional treat, not a dietary staple. More broadly, CA is comfortable that Australian cricket’s collective activity has a net positive impact in encouraging healthy and active lifestyles.

Peter Young

To the Editor: I read with interest the letter by Lim and colleagues on anorexia nervosa and senna misuse.1 I have seen abnormal whole body bone scans in patients with severe eating disorders of exactly the same pattern (except for the avid bilateral apical lung and gastric uptake) as the case described. However, I disagree with the interpretation of the bone scan. There was increased periarticular tracer uptake involving long bones. The pattern was not that of hypertrophic osteoarthropathy (HOA). The pattern in HOA is linear tracer uptake by the periosteum, particularly along the distal ends of long bones.2 The scan in the case reported did not show uptake of this pattern, despite radiological evidence showing periosteal reaction and new bone formation of the tibia and fibula at the ankle. The pattern exhibited in this patient was more consistent with metabolic bone disease (increased tracer uptake by the ends of long bones periarticularly, the axial skeleton, calvaria, mandible, sternum and “beading” of costochondral junctions, with faint, or absent, renal uptake),3 although not all of these features were present in this case. Metastatic calcification of the gastric wall (not mentioned by the authors) and upper lobes of the lung was present in this patient. Metastatic calcification of the lungs can be diffuse4 or localised (most commonly) to the upper lobes, as in this case.5 With regard to the bone mineral density results in this case, the authors state that the lumbar and femoral neck T scores were elevated (1.2 and 1.3, respectively). The normal range of the T scores is ± 1.0 standard deviation of young adult normal values.6 Elevated bone mineral density measurements are generally not of pathological significance and are therefore clinically not relevant. In my experience they are usually decreased, and are often osteoporotic, in patients with severe eating disorders.

Andrew F McLaughlin

Obesity control in Australia is imperative, and has much to learn from tobacco-control strategies The increasing incidence of obesity in Australia is set to impose a major additional cancer burden at a time when population ageing alone is projected to cause unprecedented growth in cancer incidence. While obesity is frequently associated with type 2 diabetes, hypertension, lipid abnormalities and death from heart disease and stroke, there is growing evidence for its role in causing cancer. A systematic review and meta-analysis, which included the Million Women Study, investigated the link between body mass index (BMI; calculated by dividing weight in kilograms by height in metres squared) and types of cancer.1,2 In men, a 5 kg/m2 increase in BMI was strongly associated with adenocarcinoma of the oesophagus, and thyroid, colon and renal cancers, and in women with adenocarcinoma of the oesophagus, and endometrial, gallbladder and renal cancers. There were weaker associations for melanoma and rectal cancer in men, and postmenopausal breast, thyroid and colon cancer in women. Leukaemia, myeloma and Hodgkin disease were associated in both sexes. One postulated mechanism for the link between obesity and cancer is that chronic hyperinsulinaemia results in raised levels of free IGF-I (insulin-like growth factor), with higher mean concentrations in men compared with women. This alters the environment of cells to favour cancers developing.3 In adipocytes, androgens are converted to oestradiol, and chronic hyperinsulinaemia also reduces sex-hormone-binding globulin, leaving more oestrogen to impact on oestrogen-sensitive tissues. Further, adiponectin, a protein hormone secreted by adipocytes, is an insulin-sensitising agent that is anti-angiogenic and anti-inflammatory, inversely correlated with BMI, found in higher concentrations in men than in women and, in some studies, its level is inversely associated with cancer risk.4 Obesity is linked to 11% of colon cancers and 9% of post-menopausal breast cancers5 — both increasingly common tumour types in Australia as a result of population ageing. With high percentages of endometrial cancer (39%), oesophageal adenocarcinoma (37%), kidney cancer (25%) and gallbladder cancer (24%) attributed to obesity and overweight, these rarer cancers may become more common as Australia’s obese population ages.5 The risk of an obesity-related increase in cancer burden in this country is amplified, with the link between BMI and cancer compounded by a 50% increase in the number of obese or overweight Australians over the past 15 years. An estimated 7.4 million Australians are obese or overweight, including a quarter of children aged between 5 and 16 years.6 Multiple strategies are needed to control obesity. Decreasing the consumption of energy-dense, nutrient-poor foods and encouraging consumption of healthy foods and increased physical activity are clearly the keys. What is not so obvious is what works. The high risk of childhood obesity continuing into adulthood and the lag time before the development of cancer make children a critical target for obesity-control programs. A range of interventions have been introduced, such as regulating school canteens, eliminating soft drink sales in schools, physical activity programs and education, but there is no coherent national strategy. The debate on whether such a national strategy should include restricting junk-food advertising is likely to continue for a number of compelling reasons. Australian children are exposed to more food advertising than children in the United States, United Kingdom, New Zealand and 11 western European nations,7 much of it potentially misleading in its use of healthy imagery to promote products high in sugar, fats and salt.8 Governments in Sweden, Norway and Quebec have restricted junk-food advertising to children, with some encouraging results.9 Great Britain adopted a similar policy in 2007, so more data on the efficacy of this strategy will emerge. In the absence of empirical Australian data, modelling by the Victorian Government shows that restrictions on junk-food advertising would be the most cost-effective intervention for reducing adolescent obesity.8 The South Australian Government has announced a phase-out of junk-food advertising during children’s television viewing hours, using its sovereign authority to act independently of federal broadcasting laws. Other jurisdictions may follow, and this presents an opportunity for the federal government to show national leadership towards a uniform approach. Product labelling that informs consumers in making healthier choices is also pivotal to food marketing reform, while government assistance to make healthier foods more affordable and accessible, particularly to disadvantaged groups, should also be considered. A whole-of-government response to fostering healthier communities, including initiatives to support increased physical activity, must also be built into a national obesity strategy. Consideration of the options for reducing obesity draws historical comparisons with the experience of tobacco control in the early 1970s. While minimising the use of tobacco (which has no safe consumption level) differs in many ways from reducing junk-food consumption (which is low risk if consumed in moderation), there are compelling parallels. The disease burdens related to both tobacco and obesity are disproportionately prevalent among disadvantaged population groups. Tackling both smoking and obesity requires a combination of research, policy, social marketing and program-based interventions. And, of particular interest to the debate on food advertising, there are commercial interests with a clear stake in maximising junk-food consumption, just as there are in maximising tobacco consumption. Moreover, public health advocates cite “de-normalisation” as a key to Australia’s historical success in reducing tobacco consumption. It could be argued that excessive junk-food consumption is effectively “normalised” at an early age by the sheer volume of advertising pitched at children. An important lesson from tobacco control is that an array of modest government interventions to influence healthy behaviour will fall well short of their potential if they must compete with big-budget advertising from industry encouraging unhealthy choices; smoking rates in Australia dropped markedly when broadcast advertising of tobacco was phased out in the mid 1970s.10 With an increasing incidence of cancer, now is the time for a range of tough decisions that will modify dietary behaviour and put public health before corporate interests.

Ian N Olver MD, PhD, FRACP · Paul B Grogan

Objective: To investigate the incidence of bariatric surgery and postoperative outcomes in a population-based cohort of patients in Western Australia over a 17-year period.Design and setting: A population-based incidence study of all bariatric procedures (n = 1403) performed in WA hospitals over the period 1988–2004, based on hospital morbidity and death data from the WA Data Linkage System.Main outcome measures: Changes in incidence of bariatric procedures over time; mortality and complications within 30 days after surgery; survival rates after surgery relative to age-, sex-, and period-matched survival rates in the general population; factors predictive of re-admission to hospital.Results: The incidence of bariatric surgery increased from 1.2 procedures per 100 000 person-years in 1988 to 24.2 procedures per 100 000 person-years in 2004. Although some of this was ascribed to a rising prevalence of obesity generally, there was a 13-fold increase in the bariatric procedure rate within the obese population itself. At 5 years, the relative survival rate in bariatric patients was the same as the survival rate in the general population. Within the 30-day postoperative period, mortality was low (0.07%) and 9.6% of patients experienced complications. Those who had bypass-type procedures were more likely to be re-admitted within 30 days than those who had gastric reduction procedures (adjusted hazard ratio, 5.80 [95% CI, 3.42–9.84]).Conclusion: The use of bariatric surgery increased 20-fold over the study period. Relative survival after surgery was in line with population norms. The observed low mortality rates and moderate level of complications are similar to findings in other studies in which the proportion of reduction procedures has been high.

Fiona J Smith BHlthSc(Hons) · C D’Arcy J Holman MB BS, MPH, PhD · Rachael E Moorin GradDipHlthEcon, MSc, PhD · David R Fletcher MB BS, MD, FRACS

To the Editor: We read Pham and colleagues’ recent article1 with interest, as evidence mounts against the use of probiotics in critically ill patients. Although a plausible and attractive theory, probiotics in the patient with acute illness now appear ineffective, if not positively harmful. A recent randomised trial of probiotics in 298 patients with severe acute pancreatitis showed a non-significant rise in infective complications,2 in keeping with results of previous studies of critically ill patients.3,4 Disturbingly, mortality in the probiotic group was more than double that in the placebo group (P < 0.01). Bowel ischaemia was a prominent feature of deaths in the probiotic group (eight patients), but was not associated with any deaths in the placebo group (P < 0.004). It may be that non-occlusive mesenteric ischaemia in critical illness is exacerbated by the added bacterial load itself, or through a pro-inflammatory response by gut epithelial cells. While probiotics may be a benign and beneficial adjunct to enteral feeding in certain clinical situations, there is persuasive evidence that probiotic therapy is associated with increased infective complications in critically ill patients and significant mortality in patients with severe acute pancreatitis. Until there is evidence to the contrary, we believe probiotics should not be administered to patients with severe acute illness.

Shimonti Chatterjee · John Fraser

To the Editor: Pham and colleagues commented on the effects of probiotics; however, not much is known about the impact of probiotics on weight gain and obesity. It is known that a predominance of certain bacteria, such as Lactobacillus, in the bowel can promote weight gain. Many of these bacteria are found in probiotic products. The human intestinal microbiota is predominantly colonised by the Firmicutes and Bacteroidetes phyla of bacteria. Lactobacillus and Bifidobacterium, found in a number of probiotic products, belong to the Firmicutes phylum. A study has shown that obese people carry a higher proportion of bacteria from the Firmicutes phylum and that there is a statistically significant decrease in the proportion of Firmicutes bacteria as they lose weight.3 A similar pattern of Firmicutes predominance has been found in obese mice. Furthermore, the microbiota of the obese mice were more likely than those of lean mice to break down otherwise indigestible polysaccharides from the diet.4 In other words, a higher proportion of Firmicutes bacteria was associated with increased and more efficient caloric uptake from food. These data did not necessarily imply causation, so the investigators performed another experiment. They transferred intestinal microbiota from obese and lean donor mice to germ-free mice, and found that the mice who received microbiota from the obese donors had a significant increase in body fat after 2 weeks compared with the recipients from the lean donors.4 It is therefore likely that the bacteria often found in probiotics can cause weight gain. Obesity in children and adults is a major health problem in developed nations. Given the increasing use of probiotic products in such countries, large studies should be performed to characterise the association between probiotics and obesity. Such studies may not find any association or may find that there is only a dose-related risk. If there is an association, probiotics may still prove useful in certain circumstances (eg, for weight gain in children failing to thrive).

Sanjaya N Senanayake

In reply: The comments by Chatterjee and Fraser regarding the danger of administering probiotics to patients with acute severe illnesses are important additions to the debate on the risks and benefits of probiotic administration. We also thank Senanayake for his interesting comments on the possible role of probiotics in weight gain. The recently published multicentre trial1 describing unexpected adverse events associated with probiotics in acutely unwell patients with severe pancreatitis is one example of an adverse outcome following probiotic administration. The use of probiotics in patients with severe comorbidities and in those who are immunocompromised is also contraindicated. There are reported cases of Lactobacillus GG sepsis in premature babies with short gut syndrome,2 and Saccharomyces boulardii fungaemia has been described in immunocompromised patients.3 It is interesting to note that two systematic reviews have assessed the efficacy of probiotics in prevention of necrotising enterocolitis in premature (< 33 weeks’ gestation) and very low birthweight (< 1500 g) infants.4,5 Both reviews concluded that probiotics may decrease the incidence of necrotising enterocolitis in preterm infants, and that severe adverse events were not associated with probiotics in these unwell and immunodeficient patients. However, there were insufficient data to comment definitively on the short-term or long-term safety of probiotics in these infants; this will require assessment in future large trials. The increased scrutiny of probiotics resulting from the publication of the adverse outcomes in adults with severe acute pancreatitis1 may, by necessity, slow the commencement and progression of these larger trials in infants in the neonatal intensive care setting.

Mimi Pham · Daniel A Lemberg · Andrew S Day

To the Editor: The article by Haug and colleagues on household food stockpiling is a useful contribution to a neglected aspect of disaster planning.1 However, rather than providing a guide to what foods should be stockpiled, it may be more valuable to encourage families to increase the amount and rotation of the non-perishables they currently purchase. The authors seek to promote a balanced nutritional diet, but encouraging a family to continue their usual purchasing patterns when stockpiling for a pandemic or other disaster is a simpler, more sustainable, and possibly more effective way to promote household food stockpiling. We must assume that the family currently survives, for better or worse, on their current food purchase pattern. While the article states that supermarket stocks will become depleted within 2–4 weeks, it is likely that stocks would become significantly depleted at an individual store level within 2–3 days of the last truck delivery, particularly if panic stockpiling occurs. How long interruptions to the food supply chain last will depend on the nature of the disaster, but the Australian Government Department of Health and Ageing recommends that people have “enough fluids and food on hand to last you and your family a week.”2 It does not provide guidance on how much water is required per day. This is an important issue, as mains water could be unavailable within hours to days of electricity supply outages, because electricity is required to pump water into elevated water reservoirs to maintain water pressure. People may be unaware of their daily fluid requirements and may run out of water and other potable fluids before they run out of food. The US Health and Human Services recommends a 2-week food and water stockpile (“one gallon of water per person per day”), which is roughly equivalent to four litres per person per day.3 A random household survey in the Hunter Region of New South Wales after a storm-related disaster in June 2007 revealed that over 80% of households had enough non-perishable food for 3 days, but less than 40% had enough stored drinking water for 3 days (Hunter New England Health, unpublished data). Community continuity planning should be based on an understanding of baseline household food and water reserves, and household capacity and willingness to stockpile across all social strata. Governments should actively promote household stockpiling and identify strategies to bridge the shortfall in households unable to stockpile.

Craig B Dalton · Michelle A Cretikos · David N Durrheim

In reply: Dalton et al have raised several important points for discussion. They suggest that an adequate food “lifeboat” can be procured by simply encouraging a family to continue their usual purchasing patterns. Unfortunately, accumulating non-perishable items in this way would be a fast route to certain nutritional deficiency. It is the perishable items — fruit and vegetables, bread, meat and dairy products — that supply the bulk of micronutrients in modern food supplies. Within a few short months, an individual relying on usual pantry supplies could be suffering from acute deficiencies of vitamin C, and folate and other B vitamins. Babies conceived during this period would be at risk of neurological defects. We agree that an important issue is the possibility of failure of the mains water. Indeed, many of the foods in our list require water for cooking (rice, pasta etc). Rainwater tanks and the ability to sterilise water by gas heating or chemical means may be lifesavers. We agree that governments should be actively promoting appropriate stockpiling in homes, places of employment and in areas of essential infrastructure.

Jennie C Brand-Miller · Jennifer McArthur · Anna Haug

Reducing the growing burden of food allergy requires a chronic disease management model, clarification of responsibilities, and better communication of both risks and uncertainties Food allergy and anaphylaxis are increasing in the Australian community, particularly in preschool-aged children,1,2 although, paradoxically, mortality occurs almost exclusively in school-aged children and adults.3 Food allergy and anaphylaxis are high-stakes and highly uncertain issues, where the outcome may be the sudden and unpredictable death of a child.4 The concept that a patient is “at risk” inevitably invokes uncertainty. It is possible to prospectively identify those at risk by virtue of having food allergy, but diagnostic tests are not highly predictive of anaphylaxis. The population with food allergy is substantially larger (about 10–20-fold) than the population who will experience anaphylaxis. Patients and their carers therefore live with being at risk, while not knowing exactly what the nature or extent of the risk is. In clarifying what we mean by “anaphylaxis risk”, the conventional wisdom in risk communication literature is to avoid essentially meaningless terms such as “potential risk” or “high risk” and to instead employ techniques that more accurately convey quantitative estimates of risk. This is risk as numbers, or “the probability that an event will occur, eg, that an individual will become ill or die within a stated period of time”.5 Mortality figures for food anaphylaxis in New South Wales show that the numerical risk that a teenager allergic to peanut or tree-nut will die from anaphylaxis in the next year lies between 1 in 10 000 and 1 in 100 000 — in the same order as the chance of an Australian resident being murdered in the next year.6 The risk that a child aged under 5 years will die from food anaphylaxis in the next year lies between 1 in 1 million and 1 in 10 million — the same order as the risk of death from being struck by lightning.6 However, there are problems with this numerical approach to risk assessment: the data to calculate probabilistic risk for anaphylaxis are either unavailable or not generalisable; numerically small risks are difficult to communicate; and death by lightning or violence is not necessarily viewed in the same way as a child dying from eating food. Due to its emotive characteristics, the risk of food anaphylaxis is likely to be appreciated by experiential rather than analytical cognitive processes,7 which are intuitive, automatic, and greatly influenced by associations and affect. Fear of the unpredictable death of a child may outweigh any rational consideration of its numerical likelihood. Care must therefore be taken when discussing anaphylaxis risk with patients and parents, with a key consideration being the need to sensitively communicate uncertainty as much as communicate risk. As food is essential, some exposure to risk is unavoidable. Although food labelling is becoming clearer, there are persistent uncertainties about mislabelling and cross-contamination with allergens, coinciding with broader concerns about food quality and production, and societal expectations that parents and others will provide safe food for children. Accordingly, food allergy is as much a sociocultural as a medical issue, and, for some, the constant obligation to make careful decisions about what to eat or feed their child, together with ongoing uncertainty about the risks, can create an enormous burden. Reducing this burden requires a coordinated and intersectoral response, from consumers, the health care, teaching and childcare professions, the food and pharmaceutical industries, and statutory bodies at both state and federal level. Clarification of responsibilities is required for food labelling and production, care in schools and preschools, anaphylaxis education (involving anaphylaxis recognition and risk minimisation, as well as correct use of EpiPen autoinjectors [CSL Limited, Melbourne, Vic]), and monitoring EpiPen use. It is encouraging that, in recent months, the Victorian Government has announced legislation mandating a school anaphylaxis management standard8 and the Western Australian Government has committed $6.6 million to a program of interventions.9 Nevertheless, as with other “messy” and uncertain problems, pure science and rationality alone are not sufficient.10 In formulating policy, the process of representation, clarification of common aims and interests, and debate over what we mean by “anaphylaxis risk” may be more important for developing a coherent and coordinated framework for action than would identifying an elusive “right” response. At the service provision level, there has been a tendency for medical treatment of an acute emergency to be the focus of food allergy management. Emergency treatment itself brings additional uncertainties — guidelines for EpiPen prescription leave much to individual judgement, and one study found that only 2% of doctors in a major Australian paediatric teaching hospital could correctly demonstrate all steps in EpiPen administration.11 Fortunately, despite the many uncertainties, most food-allergic patients are generally well and the EpiPen is appropriately unused. Nevertheless, it is more appropriate for food allergy, with its unpredictable “exacerbations” or reactions, and its requirement for community management of risks, to adopt a chronic disease management model, centring on self-management, patient and carer education, continuity of care and multidisciplinary services. Such an approach, including ongoing support from dietitians and nurse educators, is likely to reduce the uncertainties of daily management. The need for parent and carer education is evidenced by an Australian survey of EpiPen use, which found that only 29% of parents administered the EpiPen when indicated.12 Parental satisfaction with information provision is also associated with less seeking of second opinions.13 Thus, adequate parent and carer education and follow-up may ease pressure on referral services, which currently have 10–14-month waiting times for hospital paediatric allergy consultations. The uncertainties surrounding food allergy arise from a lack of scientific, epidemiological and personal knowledge, the need to negotiate between different sectors and interests, and ambiguous language and concepts that are difficult to communicate. Different responses are required at interpersonal, service delivery and policy levels. While some uncertainties are irreducible, patients and carers are also experiencing unnecessary uncertainties. What is certain is that food allergy has become a significant concern for public health, paediatric and general medical practice.

Andrew S Kemp MB BS, PhD, FRACP · Wendy Hu MB BS, PhD, FRACGP

Same time, another place An 8-year-old boy with marasmus presented with poor vision. His right eye had a staphyloma and his left eye a leukoma. He was totally blind in the right eye. His visual acuity in the left eye was only perception of light. Corneal transplantation for his left eye has been planned. The right eye will be enucleated and an ocular prosthesis implanted. Five years earlier, the child was admitted for treatment of kwashiorkor with associated bilateral keratomalacia due to vitamin A deficiency. These ocular sequelae of vitamin A deficiency could have been prevented by its timely supplementation. CommentaryAlthough it is no longer common in Australian Aboriginal communities, malnutrition still occurs in isolated areas. In Australia, keratomalacia of the degree shown here would be exceptional.1 In Africa and parts of south Asia, however, such causes of blindness are not uncommon, particularly among refugees from war and civil strife, where community structure is destroyed, immunisation rates (especially for measles) are low, and malnutrition is common. These circumstances are unfortunately still occurring, exacerbated by climate change, protracted drought and disruption of the normal seasonal cycles of agricultural production. Vitamin A deficiency is common even without kwashiorkor or marasmus, and keratomalacia can be precipitated by an outbreak of measles or acute diarrhoeal disease if vitamin A levels are low. Although blindness in children is far less common than in adults, blind children tend to be blind for longer and have less access to education, and are then less able to contribute to the community and the economy. Such a serious disorder can be avoided entirely by using one of the simplest and most cost-effective public health interventions: vitamin A supplementation. Vision 2020: the Right to Sight (the global initiative of the World Health Organization and the International Agency for the Prevention of Blindness to eliminate avoidable blindness and vision impairment by 2020) prioritises such devastating but needless causes of blindness. This has, through surveillance, advocacy and direct action, led to such sequelae becoming very rare in politically stable countries.

Sunil Karande · Sujit Jagtap · Richard T Le Mesurier

Three types of infant formula (soy, extensively hydrolysed and amino acid) may be appropriate for treating cows milk protein allergy. Selection of a formula depends on the allergy syndrome to be treated. Extensively hydrolysed formula is recommended as first choice for infants under 6 months of age for treating immediate cows milk allergy (non-anaphylactic), food protein-induced enterocolitis syndrome, atopic eczema, gastrointestinal symptoms and food protein-induced proctocolitis. Soy formula is recommended as first choice for infants over 6 months of age with immediate food reactions, and for those with gastrointestinal symptoms or atopic dermatitis in the absence of failure to thrive. Amino acid formula is recommended as first choice in anaphylaxis and eosinophilic oesophagitis. If treatment with the initial formula is not successful, use of an alternative formula is recommended.

Andrew S Kemp PhD, FRACP · David J Hill FRACP · Katrina J Allen FRACP, PhD · Kym Anderson FRACP · Geoffrey P Davidson FRACP · Andrew S Day MD, FRACP · Ralph G Heine MB ChB · Jane E Peake FRACP, DTM · Susan L Prescott BMedSc, PhD, FRACP · Albert W Shugg DCH, FRACGP, FRACP · John K Sinn MMed(ClinEpi), FRACP

To the Editor: The food environment in Australia and other developed countries is obesogenic. In the United States, personal-injury lawsuits against food and beverage companies are prominent, although proving the addictive nature of a food or its components is challenging. What cannot be questioned is that rates of overweight and obesity among children are increasing, and so are the associated multiple negative health and psychosocial effects.1 Given the serious health consequences of obesity, it is imperative for researchers and community groups to continually challenge the food and beverage industry to produce foods that will not impinge on the health and wellbeing of our children. The consumption of sugar-sweetened soft drinks has been linked to increasing body mass index and risk of obesity in children and adolescents.2 There are many potential reasons for this over-consumption, including aggressive marketing. However, a further contributing factor is the presence of caffeine. Caffeine is mildly addictive at low doses,3 and is an additive in cola soft drinks in Australia (concentration range, 0.55–0.67 mmol/L). Soft drink manufacturers claim caffeine is a flavour enhancer in soft drinks,4 but we have shown that caffeine has no flavour activity in a common cola soft drink (30 trained tasters completed over 1600 individual discrimination tests, and the tasters were unable to detect 0.67 mmol/L caffeine in a soft drink — if we cannot discriminate between a caffeinated and non-caffeinated sample, there is no flavour activity). A caffeine concentration of 0.67 mmol/L is equivalent to about 55 mg of caffeine in a 500 mL bottle of cola, and this dose results in physiological and psychological modifications in adults3 that manifest as behavioural modifications including increased alertness, energy, and ability to concentrate. Such positive postingestive effects are subconsciously associated with consumption of the sugar-sweetened beverage, thereby encouraging repeat consumption. Children are more likely to be affected by caffeine, and it is reasonable to assume that even lower doses of caffeine will result in behavioural modifications in children, and encourage repeat soft drink consumption. On average, 113 L of soft drink are consumed per person per year in Australia, and although not all of these beverages are caffeinated, the top sellers are cola soft drinks.6 As caffeine has been shown not to have any flavour activity in these beverages, we pose the question: given the serious nature of childhood and adolescent overweight and obesity, should caffeine be an additive in soft drinks marketed aggressively and sold to children and adolescents?

Lynn Riddell · Russell S Keast

Further progress may require business and public sector partnerships Chronic diseases in low-to-middle-income countries have continued to increase. At the same time, calls for prevention have grown.1-3 The World Health Organization resolution on diet and physical activity, published in 2004, recommended several specific actions for food companies and the broader private sector.4 Among these were: Limit the levels of saturated fats, trans fatty acids, free sugars and salt in existing products; Continue to develop and provide affordable, healthful and nutritious choices to consumers; Practise responsible marketing that supports the strategy, particularly with regard to promoting and marketing foods high in saturated fats, trans fatty acids, free sugars or salt, especially to children; Issue simple, clear and consistent food labels and evidence-based health claims; and Assist in developing and implementing physical activity programs. PepsiCo’s strategyEven though foods from PepsiCo contribute a modest proportion of calories to a typical diet in most of its markets, we believe we should continually improve nutrition so that each calorie has the optimum fat, sugar and salt content. We do so by reducing certain nutrients and increasing others. We have developed methods of measuring the current use of fats, sugar and salt in all our products in all countries where they are sold. On the basis of these measurements, we have set targets for reducing the levels of food constituents such as fats, sugar and salt by 2010. The example of trans fatty acids and our use of oils illustrates how commitment and actions need careful thought. We continue to reduce trans fatty acids in all markets and have eliminated them from virtually all our oils used for cooking potato chips and snacks. In Europe, introduction of a new oil, Sunseed, which is higher in monounsaturated fats and lower in saturated fats has led to a 50%–70% reduction in the saturated fat levels in our potato chips and snacks compared with the same products in 2005. Further progress on reducing trans fats and saturated fats awaits further research generally on alternatives to trans fats and the optimal mix of fats and oils in food products. Food companies need to ensure the long-term supply of the crops needed to produce high-quality oils. This has become increasingly complex in a world of globalised trade and when the future demand for biofuels is likely to affect the price and availability of oils. It is likely to be an even bigger problem in small and medium enterprises in low-to-middle-income countries. Public demand for reduced sugar in food and beverages has stimulated research efforts to find natural sweeteners with the same taste but fewer calories than current products. Similarly, companies are actively seeking ways to maintain taste and the other qualities that salt brings to foods with healthier alternatives or formulations. In the United Kingdom we have lowered salt levels in all packaged chips by 25% through reformulation. Further progress in the UK and elsewhere requires industry-wide collaboration and agreement on acceptable levels, supported by governments. Public health partnershipsFood industry investments in product reformulation will yield major public health gains, but product reformulation is only part of the solution. Well grounded insights into country-specific consumer preferences drive our decisions about when and how to introduce new products. We now seek ways of working with public health researchers to share our perspectives on how best to truly change the behaviour of consumers for public and private good. Our experience in the United States, for example, suggests that well designed, science-based logos can influence consumer behaviour. Sales of products that carry our Smart Spot logos (Box) are growing far faster then others, leading to more healthful consumption, and profits. To date, most of the public sector research effort in relation to obesity or diet has tended to favour medication solutions over food-based solutions. We believe a shift in focus would stimulate new partnerships between corporations and public health scientists that could lead to healthier food products being developed through innovative science — as we have seen with new pharmaceutical products. A renewed and more forward-thinking nutrition-science agenda should go beyond a focus on reducing “harms” to identifying how the global underconsumption of fruit, vegetables and cereals could be partly addressed through new products; how nutrients might enhance physical and mental performance; and ways of addressing satiety and weight management. Research partnershipsProduct reformulation is only part of the company’s solution. The PepsiCo Foundation, the primary charitable arm of the company, is deeply engaged in developing new models of partnership that will lead to health gains in communities and new research insights.5 There are still no documented successes in reducing obesity in a large community setting anywhere in the world. We are supporting research aimed at meeting this gap.6 For example, in the US, foundation support for Tufts University has helped to develop one of the few examples of a community-based approach that may reduce obesity in children.7 Internationally, we have announced support for Community Interventions for Health, a partnership with the Oxford Health Alliance.8 The partnership will carry out large-scale, community-based research projects in India, China, Mexico and the UK aiming to reduce the effects of the major risk factors for chronic diseases. Further, both the company and the foundation are involved in a range of initiatives aimed at increasing physical activity around the world in settings as diverse as Mexico (through Vive Saludable which addresses healthful eating and physical activity in primary schools) and in the US (through America on the Move). ConclusionNo single company can turn around the current threat of chronic disease. That is why we seek corporate and public sector partners. The role of the medical profession has been decisive in the battles against so many causes of ill health. This is the time, in our view, for them to review their clinical and public health roles in supporting patients and communities to tackle the major public health issue of obesity. PepsiCo is ready to join them in this task. Smart Spot product criteria Smart Spot beverage and food products: contain at least 10% of the daily value of a targeted nutrient (eg, protein, fibre, calcium, iron, vitamin A, or vitamin C); and meet the limits of the Institute of Medicine (the United States independent advisory body on health) or the US Food and Drug Administration for fat, saturated fat, sodium and added sugar; or are formulated to have specific health benefits; or are reduced in calories or nutrients like fat, sodium or sugar. This packet of chips displays the Smart Spot logo.

Derek Yach MB ChB, MPH · Antonio Lucio BA · Carlos Barroso BChemEng

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

Large catastrophes have caused the collapse of empires and civilisations.1 Science and knowledge may help prevent some catastrophes, but urbanisation and narrowly concentrated food supplies, climate change and terrorism contribute to considerable risk. Viruses responsible for severe acute respiratory syndrome (SARS) and avian influenza A (H5N1) or “bird flu” are among the most immediately identifiable risks. The World Health Organization has stated that the risk scenario associated with an outbreak of pandemic H5N1 influenza should be considered more serious than was previously assumed.2 Early self-isolation and social distancing measures are known to be highly effective.3 In the event of a lethal pandemic, emergency measures such as closing schools, staying home with family and friends, and avoiding contact with other people (until all have been immunised) will be instrumental in avoiding infection. People employed in essential services or occupations may be required to reside at their workplace for the whole period of the crisis. To achieve this type of isolation, sufficient food of adequate quality and quantity must be available. The Australian Government and the Australian Food and Grocery Council (AFGC) have been planning for such a scenario for several years and have advanced plans in place (Russell Neal, AFGC, Canberra, ACT, personal communication). Nonetheless, the logistics and practicalities of household food stockpiling should be given greater media coverage. Australia has one of the most concentrated food supplies of any country, being dominated by two large supermarket chains. These organisations operate with such efficiency that their logistic chains hold only a few weeks’ supplies (Russell Neal, AFGC, personal communication). If the supply chain shuts down, or if there is no delivery from central stores, supermarkets’ stocks will be depleted within 2–4 weeks (Clare Buchanan, Public Relations Officer, Woolworths Pty Ltd, Sydney, NSW, personal communication). If domestic stockpiling begins at this late stage, then depletion will be accelerated. Food supplies in the home will need to last as long as it takes for vaccine development and production. For ordinary seasonal influenza vaccines, there is a lag of 6 months or more after a new virus strain has first been discovered until a new vaccine is available for distribution. For weather-related catastrophes, food stockpiles might be required for much longer. A destabilised global climate, where small changes in atmospheric and ocean circulations have major consequences for temperature, rainfall, wind and storm patterns, may precipitate food stockpile dependence for several years.4 While long-term food stockpiling could be considered a governmental responsibility, we suggest that home stockpiling of food to last about 3 months might be done by individual households. This would allow a window of time for governments to put emergency action plans and food deliveries in place. Which foods and in what quantities?It is logical that the foods to be stockpiled should be staples and well accepted, easy to store, packed where possible in an inert gas for a longer shelf life, and not dependent on refrigeration. Importantly, they should be nutrient-dense, providing the recommended macronutrients and micronutrients for all members of the family.5 Ideally, they can be eaten without cooking, in case gas and electricity fail. Cost, volume and storage space are further considerations. A food stockpile should provide an average energy intake of about 9 MJ (2150 kcal) per person per day in order to avoid significant weight loss. This is near the average intake — men need a little more than women, while children need less.5 In a home quarantine situation, physical activity is not likely to be high. Box 1 shows a food “lifeboat” for one person for 10 weeks, and in Box 2, we provide an example of a food list that provides one person with 9 MJ per day for 10 weeks and covers all known nutrient needs. This example was generated using the nutrient analysis software, FoodWorks (Professional Edition 2007; Xyris Software, Brisbane, QLD), which is based on the composition of Australian foods, and commonly used by Australian dietitians. The recommended daily intake of specific macronutrients and micronutrients for adults and children is published by the Australian Government Department of Health and Ageing.5 Together, these two sources make it possible to compose diets with the appropriate quantity of nutrients. As most people have no access to detailed nutrient data, we have developed these examples to show what is needed, and typical of what might be acceptable. We acknowledge that such food lists are culturally and ethnic-specific, and that other food combinations are possible. It would be cheaper and require less storage space to rely on multivitamin tablets rather than canned fruit and vegetables to cover the requirements of vitamins such as C and A. For this reason, Box 3 shows a food list that covers basic nutrient requirements when taken together with a multivitamin–mineral supplement. Indeed, some micronutrients do not need to be consumed on a daily basis because of the capacity of the body to store them (eg, vitamin A). Our calculations allow for cooking losses. While the foods can be eaten raw, some foods taste better cooked. In the event that the electricity or gas supply fails, a gas cylinder to fuel a barbeque might make eating more enjoyable. In Australia, most people have adequate money and storage space to build up their own store of foods. For those who do not, federal, state and local governments should consider a plan to construct food stockpiles across the country. Further suggestions, recipes and guidelines are given on our website (http://www.foodlifeboat.com.au). This is a university-linked, not-for-profit initiative, developed by dietitians and public health nutritionists. 1 The food “lifeboat” for one person for 10 weeks All the foods listed in Box 2 in the quantities required are displayed. Food courtesy of Woolworths Pty Ltd. 2 Suggested food list of a daily ration for one person (providing 9 MJ per day) and purchase list for 10 weeks Food g/day kg/person for 10 weeks Milk powder, full-fat, dry* 65 4.6 Weet-Bix,† regular (breakfast cereal) 30 2.1 Pasta, regular, dry 20 1.4 Instant noodles 20 1.4 Rice 25 1.8 Dehydrated potato flakes 15 1.1 Tortilla 10 0.7 Biscuit, savoury 15 1.1 Biscuit, wholemeal 20 1.4 Oil, canola 20 1.4 Powdered soup 20 1.4 Sweet chilli sauce 10 0.7 Tomato concentrate 10 0.7 Tuna, canned 60 4.2 SPAM,‡ regular (luncheon meat) 40 2.8 Lentils, dry 20 1.4 Peas, green, canned 20 1.4 Three beans mix 50 3.5 Baked beans, canned in tomato sauce 20 1.4 Corn, canned 50 3.5 Sun-dried tomatoes 20 1.4 Milo§ (beverage base) 10 0.7 Seaweed, dried 10 0.7 Raisins 30 2.1 Honey 10 0.7 Almonds 20 1.4 Apricots, dried, raw 20 1.4 Juice, carrot 50 3.5 Juice, orange 50 3.5 Vegemite¶ (yeast extract) 2 0.1 Chocolate 30 2.1 * In case of lactose intolerance, the intake of dry milk powder may be replaced by soy protein powder. Alternatively, the milk may be fermented. † Sanitarium Australia, Sydney, NSW. ‡ Hormel Foods Corporation, Austin, Minn, USA. § Nestlé Australia, Sydney, NSW. ¶ Kraft Foods Limited, Melbourne VIC. Total daily ration provides 80 g protein and 80 g fat comprising 24 g saturated fat (31% of fat intake and 10% of energy intake), 20 g polyunsaturated fat (22% of fat intake) and 36 g monounsaturated fat (47% of fat intake). The daily cholesterol intake is 101 mg. Energy intake is 16% from protein, 34% from fat and 50% from carbohydrate. Recommended intakes of all essential nutrients are provided for women and men, except for folate (which is not adequate for women of childbearing age, so a folate supplement might be considered). The cost of this diet for 10 weeks for one person is about $500. The most expensive items are milk powder, Weet-Bix,† SPAM,‡ and chocolate. 3 A list of simple dry foods that will cover basic energy needs (9 MJ per day) and most nutrients for one person, assuming multivitamin tablets are provided, and a purchase list for 10 weeks Food g/day kg/person for 10 weeks Wheat flour, wholemeal, plain 150 10.5 Oats, raw 100 7.0 Oil, canola 25 1.8 Milk powder, dry* 65 4.6 Lentils, dry 30 2.1 Peas, split, green/yellow, dry 40 2.8 Noodles, dry 50 3.5 Vegemite† (yeast extract) 2 0.1 Fruit, mixed, dried 35 2.5 Almonds, raw 40 2.8 Multivitamin–mineral supplement One tablet One box * In case of lactose intolerance, the intake of dry milk powder may be replaced by soy protein powder. Alternatively, the milk may be fermented. † Kraft Foods Limited, Melbourne VIC. Total daily ration provides 80 g protein and 76 g fat comprising 15 g saturated fat (20% of fat intake and 6% of energy intake), 20 g polyunsaturated fat (26% of fat intake) and 41 g monounsaturated fat (54% of fat intake). The daily cholesterol intake is 43 mg. Energy intake is 16% from protein, 32% from fat and 52% from carbohydrate. Vitamins C and A would have to be taken as supplements. Otherwise, recommended intakes of all essential nutrients are provided for women and men, except for folate (which is not adequate for women of childbearing age, so a folate supplement might be considered) and iron (which is provided at a lower level than recommended). In addition, about 2 litres of water per person per day would be required. This diet costs about $250 for one person for 10 weeks. The most expensive items are dry milk powder and noodles. These food items could be packed in airtight packages filled with inert gas of a few kilograms per package, and stored in food stores throughout the country.

Anna Haug PhD · Jennie C Brand-Miller BSc, PhD, FAIFST · Olav A Christophersen · Jennifer McArthur MHPEd, APD · Flavia Fayet BSc, MNutrDiet · Stewart Truswell MD, FFPHM, FRACP

Re: “Overweight and obesity from childhood to adulthood: a follow-up of participants in the 1985 Australian Schools Health and Fitness Survey”, the letter by Alison J Venn, Russell J Thomson, Michael D Schmidt, Verity J Cleland, Beverley A Curry, Hanni C Gennat and Terence Dwyer, in the 3 September issue of the Journal (Med J Aust 2007; 187: 314-315). The Box showing the distribution of body mass index values for men and women in three different age groups showed two identical graphs of the data for men. The graphs were clearly different in the original submission, but the data supplied were incorrect. The correct graphs are shown here. Distribution of body mass index values for men and women in three different age groups* * 24–27 years, 757 men and 854 women; 28–30 years, 767 men and 807 women; and 31–34 years, 673 men and 691 women in the 20-year follow-up of the 1985 Australian School Health and Fitness Survey.

Alison J Venn · Russell J Thomson · Michael D Schmidt · Verity J Cleland · Beverley A Curry · Hanni C Gennat · Terence Dwyer

Objective: To examine whether television news and current affairs coverage of overweight and obesity frames obesity in ways that support or oppose efforts to combat obesity.Design and setting: A content and framing analysis of a structured sample of 50 television news and current affairs items about overweight and obesity broadcast by five free-to-air television channels in New South Wales between 2 May and 31 October 2005.Main outcome measures: Dominant discourses about causes of overweight and obesity; proposed solutions and location of responsibility for the problem; the age-group focus of television items; the relative prominence of stakeholders; and the aspects of obesity which attract news attention.Results: Most television items (72%) framed obesity as a problem of poor nutrition. Obesity was largely seen as the responsibility of individuals (66% of items). Just over half of news items (52%) focused only on adults while 26% focused only on children. Obesity was framed largely as a problem to be solved by individual nutritional changes, exercise and surgical and medical interventions.Conclusions: While individual lifestyle is crucial to controlling weight, the research community now recognises the importance of sociocultural and environmental factors as drivers of the obesity epidemic. However, television news portrays obesity largely as an individual problem with individual solutions centred mostly on nutrition. Media emphasis on personal responsibility and diet may detract attention from the sociopolitical and structural changes needed to tackle overweight and obesity at a population level.

Catriona M F Bonfiglioli BA(Hons), PhD · Ben J Smith BSW(Hons), MPH, PhD · Lesley A King BScPsych(Hons), MPsych · Simon F Chapman BA(Hons), PhD · Simon J Holding BA

To the Editor: The recent article by Venn et al reported that childhood overweight carries through into adult overweight and obesity, but that most obese young adults in their study were “healthy” weight as children in 1985.1 As demonstrated by National Health Surveys, age is one of the strongest predictors of overweight,2 with body mass index (BMI) increasing as we grow older. However, there are two additional time-related components influencing obesity. Since 1985 (when Venn et al reported the prevalence of overweight and obesity in children was less than 10%), the environment appears to have become more obesogenic — a 2004 survey in New South Wales showed that 26% of children were overweight or obese.3 It is not only children who are vulnerable — the percentage of overweight adult Australians increased for almost all age groups from 1990 through 2001, and the mean BMI at which Australians enter adulthood has increased with each subsequent survey. For example, for women aged 20–24 years, mean BMI increased from 22.1 kg/m2 (1990) to 22.5 kg/m2 (1995) to 23.2 kg/m2 (2001) to 23.3 kg/m2 (2004). As the heights and weights were self-reported in these surveys, true BMI values may be even higher. We recently reported that year of birth (birth cohort) also predicts prevalence of overweight and obesity, independent of age and survey period; the prevalence of overweight and obesity in adults increased progressively with birth cohorts born since 1960.4 This birth span includes the cohort in the study by Venn et al.1 While obesity begins in childhood for only a small proportion of adults, the so-called healthy weight children now have a higher mean BMI, giving little margin for the seemingly inevitable increases in weight with ageing, before the population mean BMI reaches the cutpoint for overweight and later obesity. The 2004–2005 National Health Survey showed that men reached the overweight cutpoint at 25–29 years and women reached it at 30–34 years.5 Given increasing child and adult obesity, the need for allocation of public health resources to improve dietary and physical activity habits is undisputed. However, these data1,4 indicate that efforts should be directed to the hard-to-reach group, young adults, to prevent weight gain at this point. This will pose considerable challenges, because this group has minimal contact with health services, and perceives the threat of chronic illness as irrelevant. However, swift intervention is required, not only for their own health and that of their children as they become parents, but also because they will become overconsumers of health care for chronic diseases within a generation.

Margaret A Allman-Farinelli · Lesley King · Adrian E Bauman

In reply: Allman-Farinelli et al make an important point about the influence of age, survey period and cohort effects on the prevalence of overweight and obesity. While age and cohort effects could not be clearly separated in the 1985 Australian Schools Health and Fitness Survey, the prevalence of overweight and obesity increased with age in 7–15-year-olds.1 Our data collected from 4571 of the individuals in that survey at follow-up about 20 years later also showed an increase in the prevalence of overweight and obesity with age, although these findings were not presented in our report.2 In the Box, we show the distribution of body mass index (BMI) values for men and women in three age groups (24–27 years, 28–30 years and 31–34 years). Mean BMI values across the age groups were 25.2 kg/m2, 25.6 kg/m2, and 26.5 kg/m2 in men and 23.5 kg/m2, 24.2 kg/m2, and 24.6 kg/m2 in women. The prevalence of obesity (BMI ≥ 30 kg/m2) increased with increasing age as follows: age 24–27 years — men 12.2%, women 9.9%; age 28–30 years — men 12.3%, women 12.0%; and age 31–34 years — men 15.6%, women 14.6%. Distribution of body mass index values for men and women in three different age groups* * 24–27 years, 757 men and 854 women; 28–30 years, 767 men and 807 women; and 31–34 years, 673 men and 691 women in the 20-year follow-up of the 1985 Australian Schools Health and Fitness Survey.

Alison J Venn · Russell J Thomson · Michael D Schmidt · Verity J Cleland · Beverley A Curry · Hanni C Gennat · Terence Dwyer

Objective: To measure the prevalence of overweight, obesity and the metabolic syndrome (MetS) in rural Australia.Design, setting and participants: Cross-sectional surveys were conducted in two rural areas in Victoria and South Australia in 2004–2005. A stratified random sample of men and women aged 25–74 years was selected from the electoral roll. Data were collected by a self-administered questionnaire, physical measurements and laboratory tests.Main outcome measures: Prevalence of overweight and obesity, as defined by body mass index (BMI) and waist circumference; prevalence of MetS and its components.Results: Data on 806 participants (383 men and 423 women) were analysed. Based on BMI, the prevalence of overweight and obesity combined was 74.1% (95% CI, 69.7%–78.5%) in men and 64.1% (95% CI, 59.5%–68.7%) in women. Based on waist circumference, the prevalence of overweight and obesity was higher in women (72.4%; 95% CI, 68.1%–76.7%) than men (61.9%; 95% CI, 57.0%–66.8%). The overall prevalence of obesity was 30.0% (95% CI, 26.8%–33.2%) based on BMI (≥ 30.0 kg/m2) and 44.7% (95% CI, 41.2%–48.1%) based on waist circumference (≥ 102 cm [men] and ≥ 88 cm [women]). The prevalence of MetS as defined by the US National Cholesterol Education Program Adult Treatment Panel III 2005 criteria was 27.1% (95% CI, 22.7%–31.6%) in men and 28.3% (95% CI, 24.0%–32.6%) in women; based on International Diabetes Federation criteria, prevalences for men and women were 33.7% (95% CI, 29.0%–38.5%) and 30.1% (95% CI, 25.7%–34.5%), respectively. Prevalences of MetS, central (abdominal) obesity, hyperglycaemia, hypertension and hypertriglyceridaemia increased with age.Conclusions: In rural Australia, prevalences of MetS, overweight and obesity are very high. Urgent population-wide action is required to tackle the problem.

Edward D Janus MD, PhD · Tiina Laatikainen MD, PhD · James A Dunbar MD · Annamari Kilkkinen MSc, PhD · Stephen J Bunker PhD · Benjamin Philpot BSc, GradDip (Actuarial Studies) · Philip A Tideman MB BS · Rosy Tirimacco BSc · Sami Heistaro MD, PhD

To the Editor: Growth charts are important tools in assessing the physical development of infants and children. Understanding and comparing the derivation and applicability of the new World Health Organization Child Growth Standards1 and the Centers for Disease Control and Prevention (CDC) growth charts2 is essential. Arguments for and against the standard use of the new WHO growth charts are being discussed on the basis of differences in study designs used and growth patterns found.3,4 The WHO charts show the growth of breastfed infants on the basis of data from about 8500 children from widely different ethnic backgrounds and cultural settings (Brazil, Ghana, India, Norway, Oman and the United States); these children were from selected populations in which no health, environmental or economic constraints on growth existed.1 In contrast, the CDC charts represent the combined growth pattern of artificial-formula-fed and breastfed infants in the United States, where about 50% of infants are never breastfed and only around 33% are breastfed for 3 months or longer.2 Is it possible to misdiagnose breastfed infants who are growing normally as failing to thrive if the CDC growth charts are used? The simplest common definitions used for failure to thrive are a drop below the 3rd or 5th percentile for weight, or when growth deviates from an established growth curve for 3 consecutive months.5 By the CDC growth charts, the normal growth pattern described by the WHO Child Growth Standards for a 15th percentile, breastfed, female infant at 18 months would meet all three definitions of failure to thrive. The clinical response to this perceived failure to thrive may be to provide additional energy in the form of energy-dense foods or supplements (eg, artificial formula). This would at best be unnecessary, and at worst might contribute to the development of overweight and obesity. So, where to from here? We recommend that all health professionals who use growth charts be cognisant of which chart they are using and its application, especially for breastfed infants. There is also a need for Australian national and state governments to debate which growth charts should be used and in what contexts. Finally, irrespective of the choice of growth charts, it must be recognised by practitioners and the general public that these charts are guides only, and should be used as part of a holistic approach to infant growth assessment and management.

Barbara Radcliffe · Jan E Payne · Helen Porteous · Simone G Johnston