Metabolic diseases

To the Editor: Allergen avoidance is the mainstay of food allergy management. Consumers with food allergies rely on accurate labelling of foods to avoid ingestion of allergens and subsequent allergic reactions. Current Australian legislation states that ingredients derived from common allergens (peanuts, tree nuts, eggs, wheat, cows milk, soy, fish, shellfish and sesame) must be clearly labelled.1 However, use of shared processing facilities can result in cross-contamination of other ingredients with these allergens. This has led to the use of advisory statements such as “may contain traces of” by manufacturers. A recent Food Standards Australia New Zealand survey found that consumers with food allergies are frustrated by such labelling.2 There is also confusion among the medical profession about whether to advise patients with food allergies to avoid all foods with allergen avoidance advisory statements. The perception by some in the general population and in the medical community is that these statements are so widely used that avoidance would be overly prohibitive. However, there are currently no published data on the extent of advisory labelling use in Australia. We aimed to assess the prevalence of advisory labelling for three common food allergens — peanuts, tree nuts and eggs — on the packages of products for which these allergens were not listed as ingredients. Products containing one type of tree nut (eg, macadamia nut) could still have advisory labelling for other tree nuts (eg, almond). All products were therefore examined for advisory labelling for any tree nut which was not listed as an ingredient. Packages of non-refrigerated processed foods were examined between August and September 2008 at a large supermarket in Melbourne. All product types were examined within each category (eg, for the savoury biscuits category, we examined rice crackers, flavoured wheat crackers and water crackers) and, for each product type, one flavour per brand was selected for examination. Single-ingredient foods, such as flour, sugar, fruit and vegetables, were excluded. Advisory statements included, but were not limited to, “may contain traces of”, “processed on the same line as” and “made on equipment that also processes”. Overall, 761 products were examined. Of these, 384 (50%) carried an advisory statement for one or more tree nuts. Of 737 products that did not list peanut as an ingredient, 348 (47%) carried an advisory statement regarding peanut. Of 641 products that did not list egg as an ingredient, 146 (23%) carried an advisory label for egg. The presence of advisory statements varied between categories of food, with sweet biscuits most likely to carry labelling for peanut and tree nuts and bakery items most likely to carry labelling for egg (Box). Advisory statements have been widely adopted by manufacturers across a range of products, and are likely to limit food choices for consumers with food allergies who avoid all foods labelled with advisory statements. Unfortunately, there is no evidence on the frequency of trace allergen contamination in Australian products, although studies in the United States found that only 10% of 179 products with advisory labelling for peanut contained detectable levels3 and that, as for Australia, this labelling was widely used for some product categories.4 There is also no evidence regarding the proportion of consumers with food allergies who will develop an allergic reaction (including anaphylaxis) to trace contamination of food. Scientific assessment of the risks posed to consumers with food allergies by trace contamination is urgently required. This evidence would allow the development of informative labelling guidelines, including changes to legislation where required, to allow consumers with food allergies to safely manage their allergies, hopefully without the need to avoid entire categories of common foods. Allergen avoidance advisory statements on packaged processed foods at a large supermarket in Melbourne, August–September 2008 Number (%) of products with an advisory statement* Category of food Peanut Tree nuts Egg Sweet biscuits (n = 130) 117 (93%) 120 (92%) 48 (70%) Chocolates (n = 60) 43 (80%) 49 (82%) 2 (4%) Bakery items (eg, cakes) (n = 35) 24 (71%) 30 (86%) 10 (71%) Muesli bars and snack bars (n = 27) 13 (67%) 20 (74%) 4 (15%) Dinner bases and stocks (n = 32) 19 (59%) 9 (28%) 5 (17%) Savoury biscuits (n = 41) 23 (56%) 23 (56%) 20 (51%) Lollies (n = 55) 29 (56%) 25 (45%) 1 (2%) Breakfast cereals (n = 63) 25 (41%) 37 (59%) 3 (5%) Instant noodles (n = 18) 7 (39%) 6 (33%) 8 (50%) Pasta sauces (n = 15) 5 (33%) 4 (27%) 0 Bread (n = 16) 5 (31%) 5 (31%) 5 (31%) Soups (n = 20) 3 (15%) 3 (15%) 4 (21%) Cake mixes (n = 30) 4 (13%) 20 (67%) 11 (58%) Tinned meals (n = 17) 2 (12%) 2 (12%) 1 (7%) Baby foods (n = 30) 3 (10%) 3 (10%) 1 (4%) Pasta (n = 13) 0 0 4 (39%) Chips (n = 20) 0 0 0 Other (eg, tinned fish, breadcrumbs, sauces, custard powder) (n = 139) 26 (19%) 28 (20%) 19 (14%) * Number of products that had an advisory statement but did not have the allergen of interest listed as an ingredient. The denominators used to calculate percentages were the numbers of products within each category of food that did not have the allergen of interest listed as an ingredient.

Jennifer J Koplin · Nicholas J Osborne · Katrina J Allen

To the Editor: I refer to the article by Gallego and colleagues in the 19 April 2010 issue of the Journal,1 which stated that (as at the time of writing, in July 2009) Australia had no formal policies for iodine supplementation in pregnant and lactating women. In January 2010, the National Health and Medical Research Council (NHMRC) released a public statement, Iodine supplementation for pregnant and breastfeeding women.2 The NHMRC recommends that women who are pregnant, breastfeeding or considering pregnancy take an iodine supplement of 150 μg each day; and women with pre-existing thyroid conditions should seek advice from their medical practitioner before taking a supplement. The public statement also provides information on the increased need for iodine during pre-pregnancy, pregnancy and breastfeeding, the risks of not having enough iodine and the types of supplement that should and should not be used. The statement was developed in consultation with an expert reference group and was based on a review of recent international scientific literature for the efficacy of iodine supplementation in increasing iodine levels in pregnant and breastfeeding women to levels that mitigate the risks associated with iodine deficiency.3 The public statement and supporting literature review can be found on the NHMRC website.2,3

Warwick P Anderson

To the Editor: We disagree with the opinion expressed by Gallego and colleagues that Australian “women planning a pregnancy and pregnant and lactating women should be advised to take an iodine supplement”,1 and offer two reasons to support our view. First, the data suggesting mild iodine deficiency in Australian women were collected from opportunistic samples of women not representative of the population at large and were obtained before the introduction of mandatory iodine fortification of bread in October 2009. We believe that recommending iodine supplementation in pregnancy without evaluating the effect of mandatory iodine fortification on iodine intake and status of pregnant women in Australia is premature.2 This is supported by a recent report, developed by the Dietitians Association of Australia on behalf of the National Health and Medical Research Council (NHMRC).3 The report clearly shows that the recommended iodine intake for pregnant women (recommended dietary allowance, 220 μg/day) is achievable from foods alone, together with iodine fortification of bread. Second, there are no randomised controlled trials (RCTs) that have examined the effect of iodine supplementation of pregnant women from regions of mild iodine deficiency (as in Australia) on neurodevelopment of the offspring or any other clinical outcomes. Gallego et al state that “iodine-containing supplements consistently benefit the iodine and thyroid status of both mother and newborn”, citing a review of iodine supplementation of pregnant women from populations with mild-to-moderate iodine deficiency.4 In fact, none of the six RCTs included in that review showed a clear effect of supplementation on maternal and newborn thyroid hormone concentrations, which suggests that the maternal thyroid is able to adapt to meet the increased thyroid hormone requirements of pregnancy in areas of mild-to-moderate iodine deficiency.5 Furthermore, Gallego et al cite no evidence to support their statement “Even subclinical hypothyroidism in the mother, occurring as a consequence of iodine deficiency, can cause irreversible brain damage in the fetus . . .”. In our view, major public health recommendations advising routine iodine supplementation for women planning a pregnancy, as well as pregnant and lactating women, should await the results of current RCTs6-8 examining the effect of maternal iodine supplementation on longer-term maternal health and neurodevelopmental outcome of children in regions with mild-to-moderate iodine deficiency, including Australia and New Zealand.

Shao J Zhou · Sheila A Skeaff · Philip Ryan · Maria Makrides

In reply: While Zhou and colleagues disagree with our viewpoint that Australian “women planning a pregnancy and pregnant and lactating women should be advised to take an iodine supplement”,1 we note that they suggest any such recommendation should await the results of their planned randomised controlled trial (RCT) examining the effects of maternal iodine supplementation on maternal health and neurodevelopmental outcome of the offspring. They neglect to mention that the National Health and Medical Research Council (NHMRC) issued a public statement in January this year, with supporting evidence attached, stating that: “The NHMRC recommends that all women who are pregnant, breastfeeding or considering pregnancy take an iodine supplement of 150 μg each day”.2 Similar recommendations, based upon available scientific evidence, have been issued by the World Health Organization, International Council for Control of Iodine Deficiency Disorders, American Thyroid Association and American Endocrine Society. We agree that there is a paucity of RCT evidence examining the effect of iodine supplementation of pregnant women living in mildly iodine-deficient areas, and this is regrettable. Given the overwhelming animal and human evidence that maternal iodine deficiency causes brain damage in the offspring of deficient mothers, we consider there are major ethical issues in conducting such trials where pregnant women would be deprived of iodine and their babies put at risk of brain damage. Zhou and colleagues imply that mild-to-moderate iodine deficiency is not widely prevalent in Australia. This statement ignores the evidence from several clinical studies of pregnant women in New South Wales, Victoria and Tasmania, all showing that mild-to-moderate iodine deficiency is widespread in the majority of the Australian population. Analysis of the data in some of these studies shows between 20% and 40% of women tested are moderately to severely iodine deficient.3 Furthermore, food modelling studies by Food Standards Australia New Zealand (FSANZ) predict between 45% and 75% of Australian women will continue to be iodine deficient after the mandatory use of iodised salt in bread that commenced in October 2009.4 Finally, we disagree with their assertion that the recommended iodine intake for pregnant women can be achieved by the majority of women from foods alone, together with iodine fortification of bread. A trial of bread fortification in Tasmania showed this was not achievable.5 If this were achievable, it is questionable why Zhou and colleagues would even consider conducting an RCT of maternal iodine supplementation in pregnant women in Australia and NZ.

Gisselle Gallego · Stephen Goodall · Creswell J Eastman

To the Editor: We read with interest the article by Cleland and colleagues describing an urban–rural comparison of weight status among women living in socioeconomically disadvantaged neighbourhoods.1 After adjusting for socio-demographic factors, the authors reported no difference in prevalence of obesity, determined using women’s self-reported height and weight, between urban and rural areas. We would like to provide further evidence for the suggestion that obesity might be attributable to sociodemographic composition of areas. We have previously examined the association between area-based socioeconomic status (SES) and different measures of obesity in a randomly selected, population-based female cohort (aged 20–93 years, 77% participation)2 and in a similarly recruited male cohort (aged 20–96 years, 67% participation)3 within the Barwon Statistical Division in Victoria. An inverse association between SES and obesity was observed for both sexes,2,3 and was evident across three different SES indices developed by the Australian Bureau of Statistics (ABS).4 Within our female cohort, we investigated body mass index (BMI) in urban versus rural areas across the SES continuum, for 192 participants aged 20–45 years. We used standard geographical classification5 of 2006 ABS Census data to define participants’ residences as urban or rural (incorporating rural and semi-rural areas). Participants were further grouped according to the 2006 ABS Index of Relative Socio-economic Disadvantage, based on Barwon Statistical Division cutpoints. In our multivariable regression analysis, SES was categorised into the lower 30% (most disadvantaged), mid 40%, and upper 30% (least disadvantaged). Approval for this analysis was obtained from the Barwon Health Human Research Ethics Committee. No differences in unadjusted BMI were observed between participants residing in urban and rural areas (Box). These results were sustained after adjusting for age (data not shown). No interactions were identified between SES and urban or rural residence. No differences in BMI between urban and rural residence were observed for any SES group. These data suggest the lack of difference in BMI between urban and rural residents may be consistent across the SES spectrum. SES was associated with BMI (P = 0.001), while urban–rural residence was not (P = 0.5). Given these data, we suggest that SES is a stronger driving force for BMI than urban or rural residence. In our population, participants in the most disadvantaged group were more likely to be resident in urban areas. This is indicative of Geelong, the main urban centre of the Barwon Statistical Division, being one of the largest public housing areas in Victoria; urban areas provide more low-cost housing options than do rural areas. In contrast, residence in rural areas may be influenced by factors such as the “sea change” movement or prestigious real-estate options, such as the scenic coastal areas located away from the urban centre of Geelong. Mean body mass index (95% CI) of 192 women aged 20–45 years in the Barwon Statistical Division, Victoria, by area of residence Socioeconomic status* Urban† Rural† P‡ Lower 30% (most disadvantaged) 29.5 (26.8–32.1) 37.4§ 0.3 Mid 40% 27.8 (26.1–29.4) 25.3 (21.8–28.9) 0.2 Upper 30% (least disadvantaged) 25.5 (21.2–29.7) 25.5 (24.1–26.9) 1.0 Total population 27.3 (26.3–28.4) 26.1 (23.4–28.7) 0.43 * Defined by the Australian Bureau of Statistics (ABS) Index of Relative Socio-economic Disadvantage of the Socio-economic Indexes for Areas using 2006 Census data, and cutpoints of Barwon Statistical Division for 2006. † Defined by the 2006 ABS Australian Standard Geographical Classification Urban Centres/Localities. ‡ For pairwise difference. § There was only one participant in this category.

Sharon L Brennan · Margaret J Henry · Geoffrey C Nicholson · Julie A Pasco

To the Editor: At the risk of appearing self-serving, we refer to our recently published article in which we recommended that there should be “greater uniformity in [food] packaging design, colour and descriptions”.1 In light of the Australian Government’s recent mandate on plain packaging for tobacco products,2 we can see no reason why this should not be extended to processed foods possessing no redeeming nutritional qualities. This would include soft drinks, potato chips, a great many of the so-called foods offered as replacements for fruit in children’s school lunches, biscuits and sweets. We challenge the Prime Minister and Minister for Health to do this, or explain why they won’t.

Bebe Loff · Brad R Crammond

Incorrect units: In “Impact of income management on store sales in the Northern Territory” in the 17 May 2010 issue of the Journal (Med J Aust 2010; 192: 549-554), there were errors in Box 2 under the column heading “Outcome measures”. The units for “Fruit and vegetable turnover” should have been kg, and the units for “Soft drink turnover” should have been L.

Julie K Brimblecombe · Joseph McDonnell · Adam Barnes · Joanne Garnggulkpuy Dhurrkay · David P Thomas · Ross S Bailie

Recent research has confirmed that Australian children and pregnant women are mildly iodine deficient. A considerable proportion of the pregnant population is moderately to severely iodine deficient. Even subclinical hypothyroidism in the mother, occurring as a consequence of iodine deficiency, can cause irreversible brain damage in the fetus, making it essential to avoid iodine deficiency in pregnancy. The proposal of Food Standards Australia and New Zealand (FSANZ) — Mandatory Iodine Fortification for Australia (P1003) — has been implemented. FSANZ openly admits P1003 is inadequate for covering the needs of pregnant women. Therefore, health professionals and the public must be properly informed about the limitations of this proposal. Views differ about the most effective measures to prevent iodine deficiency in Australia. We propose that women planning a pregnancy, and pregnant and lactating women should be advised to take an iodine supplement. Women with pre-existing thyroid disease should exercise caution and seek medical advice before taking a supplement.

Gisselle Gallego BPharm, PhD · Stephen Goodall BSc, MSc(Health Econ), PhD · Creswell J Eastman MD, FRACP, FAFPHM

Because of the complex aetiology of modern obesity patterns, isolated therapeutic or public health measures will not solve the obesity problem. Consumers must be made aware of the ways in which the food industry influences their food purchases. Government needs to prioritise health ahead of industrial productivity and increased consumption. An obesity intervention wish list is presented as a suggested reform package: prohibit all forms of marketing of energy-dense, nutrient-poor foods; introduce measures such as kilojoule caps, prohibition of bundling, and greater uniformity in packaging design to make energy-dense, nutrient-poor foods less enticing and less amenable to bulk purchase; redesign supermarkets to promote fresh rather than energy-dense, nutrient-poor foods; cease provision of government subsidies to food processing industries; tax energy-dense, nutrient-poor foods to create a disincentive to purchasing of these foods; and regulate the location and number of fast-food outlets by enacting urban planning laws

Bebe Loff LLB, MA(Lond), PhD · Brad R Crammond MA(Hons), LLM

The recent interest in health promotion and disease prevention has drawn attention to the role of the alcohol and junk-food industries. Companies supplying, producing, advertising or selling alcohol or junk food (ie, foods with a high content of fat, sugar or salt) do so to generate profits. Even companies marketing “low-carbohydrate” beers, “mild” cigarettes, or “high-fibre” sugary cereals are not primarily concerned about population health, more so increased sales and profits. In a competitive market, it is assumed that consumers make fully informed choices about costs and benefits before purchasing. However, consumers are not being fully informed of the implications of their junk-food and alcohol choices, as advertising of these products carries little information on the health consequences of consumption. We propose that there should be a levy on advertising expenditure for junk food and alcoholic beverages to provide an incentive for industry to promote healthier products. Proceeds of the levy could be used to provide consumers with more complete and balanced information on the healthy and harmful impacts of food and alcohol choices. Our proposal addresses two of the greatest challenges facing Australia’s preventable disease epidemic — the imbalance between the promotion of healthier and unhealthy products, and securing funds to empower consumer choice.

Todd A Harper BEcon, PGDipHealthProm, MHealthEcon · Gavin Mooney DSocSc(hc)

Objective: To compare the weight status of women and children living in socioeconomically disadvantaged rural and urban neighbourhoods in Victoria.Design, setting and participants: Cross-sectional study of data collected between August 2007 and July 2008 as part of the Resilience for Eating and Activity Despite Inequality (READI) study. Women aged 18–45 years living in 40 rural and 40 urban socioeconomically disadvantaged Victorian areas were surveyed by postal questionnaire. Data from a subset of their children aged 5–12 years were also analysed. Weight and height were self-reported for women and measured for children.Main outcome measures: Women’s weight status based on body mass index (BMI): underweight; healthy; overweight; or obese Class I, II or III; children’s weight status based on International Obesity Taskforce BMI cut-off points.Results: Of 11 940 women randomly selected, 4934 (41%) replied to a postal invitation to participate. After exclusions for various reasons, data were available on 3879 women and 636 of their children. Twenty-four per cent of urban and 26% of rural women were classified as overweight; a further 19% of urban and 23% of rural women were classified as obese. Twenty per cent of both urban and rural children were classified as overweight; a further 10% of urban and rural children were classified as obese. In crude analyses, rural women had higher odds of Class I and II obesity (odds ratio [OR], 1.34 and 1.72, respectively) compared with urban women. After adjusting for sociodemographic factors (age, number of children, country of birth, education level, employment status and marital status), there was no difference between urban and rural women in odds of overweight or obesity Class I, II or III. No significant urban–rural difference in odds of overweight/obesity was evident among children.Conclusions: The higher prevalence of obesity in rural women compared with urban women was largely explained by individual-level sociodemographic factors, such as age, number of children, country of birth, education level, employment status and marital status. This suggests that higher obesity levels among women in rural areas may be attributable to the sociodemographic composition of these areas.

Verity Cleland PhD · Clare Hume PhD · David Crawford PhD · Anna Timperio PhD · Kylie Hesketh PhD · Louise Baur MB BS, PhD · Nicky Welch PhD · Jo Salmon PhD · Kylie Ball PhD

Objective: To measure the level of functional health literacy (FHL) in an Australian population, and to explore the level of risk associated with level of FHL.Design, setting and participants: Cross-sectional, random population survey administered to 2824 South Australians aged ≥ 15 years, September – October 2008.Main outcome measures: Newest Vital Sign as a measure of FHL, self-reported general health status, and use of health services.Results: 24% of respondents were at risk of limited FHL, and 21% had a high likelihood of inadequate FHL; this increased with age (≥ 65 years, 50% v 25–44 years, 11%). In multiple logistic regression models, a high likelihood of inadequate FHL was significantly more common among those with lower education (left school ≤ 15 years of age, odds ratio [OR], 8.1; 95% CI, 4.8–13.6); with lower annual income (< $20 000, OR, 4.1; 95% CI, 2.3–7.4); who were born in countries other than Australia, New Zealand, the United Kingdom and Ireland; and with poorer health status (OR, 1.6; 95% CI, 1.2–2.2). Inadequate FHL was significantly less common among females (OR, 0.6; 95% CI, 0.5–0.8). People with inadequate or at-risk FHL were significantly more likely to report having diabetes, cardiac disease or stroke, and significantly less likely to have recently attended a doctor. Respondents aged ≥ 65 years with inadequate FHL were more likely to have been admitted to hospital (OR, 2.2; 95% CI, 1.1–4.5).Conclusion: Many Australians are likely to have limited health literacy, and this is a risk to effective health care delivery and health improvement across the community.

Robert J Adams MD, FRACP · Sarah L Appleton BSc · Catherine L Hill MD, BS, FRACP · Mark Dodd BEc · Christopher Findlay BEc, MEc, PhD · David H Wilson MPH, PhD

To the Editor: The article by Calver and colleagues on the use of gastrostomy tubes in older Western Australians raises important issues regarding decision making for gastrostomy tube insertion and ongoing care of gastrostomy-fed patients. Calver et al report a high incidence of readmissions within 1 year for gastrostomy tube replacement or gastrostomy-related complication (25%) and a high 1-year mortality rate (54%)1 Extrapolation of New South Wales data suggests that about 11 000 Australians rely on gastrostomy feeding at home as their sole source of nutrition and hydration.2 In NSW, about 2300 gastrostomy and jejunostomy procedures are performed each year in public health care facilities, for which about 60% of patients are discharged home. Of these patients, 40% require tube feeding for 2 or more years, and 11% for 5 or more years. In the financial year 2004–05, there were about 700 reported presentations to emergency departments of patients requiring percutaneous endoscopic gastrostomy tube replacement or experiencing tube-associated feeding complications (eg, stoma site infection, tube blockage, buried bumper syndrome, and diarrhoea related to tube feeding); 15% of these presentations resulted in ward admission.2 Many complications can be prevented or treated effectively in the community, provided that patients, carers and health professionals are adequately trained and supported, and that formula, consumables and equipment are affordable. Of particular concern are situations where patients who have multiple comorbidities and disabilities and who cannot advocate for themselves are discharged to nursing homes and group homes. The NSW Ombudsman reported the deaths of two people in 2006 as a result of poor management of their gastrostomy tube feeding and recommended that minimum care standards be introduced.3 Enteral nutrition is an orphan therapy, with no single professional group taking ownership of it. Hospitals release their responsibility when they discharge a patient, as the patient is no longer admitted, and there are limited community services to take over care. Patients are left to fend for themselves, resulting in poor outcomes. How a patient will manage tube feeding at home should be an important part of the decision-making process that occurs before a tube is inserted, rather than an afterthought. As the use of therapies that can be performed at home increases (eg, dialysis and enteral nutrition), there needs to be increased investment in community-based health services to support patients in caring for themselves at home. This will bring social and economic benefits to both patients and the health care system.

William H Watt · Kate A Needham · Peter L Talbot · Janet P Bell · Glen J Pang

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

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

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

Barbara Depczynski

To the Editor: We read with interest the article by Alexander and colleagues on child protection issues in severe childhood obesity.1 With one quarter of Australian youth either overweight or obese, individual families (or the health care system) will not benefit from widespread involvement of child protection services in obesity. The authors are clear on this, and describe their case as “sufficiently extreme”. The difficulty lies in defining what is “extreme” and, as health professionals, we have a duty to the community to emphasise that these kinds of cases rarely occur. The illustrative case in the article by Alexander and colleagues required an amalgamation of details from several patients (for confidentiality purposes), and we believe it would be very unusual for a 40 kg 4-year-old girl to exhibit the degree of obesity-related comorbidity described.2,3 Such a degree of “medical urgency” is usually absent when managing young obese children and, in our experience, is thankfully very extreme and markedly different from the more usual scenario of discussions around potential long-term health problems. Also, there are currently no fail-safe mechanisms in place to be 100% certain that there is not an underlying genetic, hormonal or metabolic reason for continuing weight gain in a young child. With the childhood obesity pandemic, it is impossible to routinely investigate all obese youth and, even if it were, research teams are continually finding new causes for why some children continue to gain weight irrespective of lifestyle change. Indeed, the more severe the obesity, the more likely for there to be an organic cause.4 It is not in anyone’s interests for child protection services to be automatically involved because of standard recommendations when, at a later date, an underlying medical cause is discovered. Alexander and colleagues should be congratulated on re-igniting a public discussion on this highly emotive and difficult area of health care. We agree that parenting styles may influence weight regulation in young children5 but, for the above reasons, we would urge extreme caution when considering that parents may be “neglectful”. Within our obesogenic environment, perhaps (deliberate or intentional) non-compliance is an indication that society is neglecting parents, rather than that parents are medically neglecting their children? We are concerned that the development of child protection guidelines will alienate parents and families, leading to a decline in the uptake of programs aimed at preventing and/or treating overweight and obesity. We would recommend that each case be taken on its individual merit and that primum non nocere is as important as Aristotle’s phrase of “practical wisdom”.

Matthew A Sabin · Zoe McCallum · Kay Gibbons · George A Werther · Joseph Proietto

In reply: Primum non nocere means both “first, do no harm” and “above all, do no harm”. We acknowledge there may be both potential harms (the most significant being removal of the child from the family) as well as hoped-for benefits in involving child protection services in cases of severe childhood obesity. Though we strenuously oppose notification of child protection authorities as a general policy, we raised the idea that, in exceptional circumstances, health care professionals may nonetheless have a professional and legal obligation at least to consider notifying such authorities. We did so cautiously because we fear an exception becoming a rule, particularly in services such as ours where we frequently care for children very like the “child” we describe. We agree that the development of obesity usually has multifactorial causes which will include a genetic element. We also agree on the need for public health approaches to the prevention of childhood (and adult) obesity. But whatever the underlying cause of severe obesity in a particular case, and especially in circumstances where parents seem unable to attend to the physical needs of their child, health professionals have an obligation to consider all reasonable means to limiting excess weight gain.

Shirley M Alexander · Louise A Baur · Roger Magnusson · Bernadette Tobin

Economic interventions to improve access to healthy food Poor nutrition is a major determinant of excess morbidity and mortality among Aboriginal and Torres Strait Islander peoples,1 contributing to over 16% of the burden of disease.2 In this issue of the Journal (page 549), consistent with the “economics of food choice” theory,3 Brimblecombe and O’Dea report that the diet of a remote Aboriginal community was high in energy-dense, nutrient-poor foods — the cheapest options to satisfy hunger.4 This energy–cost differential restricts access to healthy food, and helps explain the persistently poor dietary patterns and deplorable health status of remote Indigenous communities.4 Placing nutrition issues in an economic framework highlights the investment required to improve Indigenous nutrition.4 But what has been learned to date about where resources should be directed? Despite the high costs and limited availability of healthy foods in remote community stores, surprising achievements have been made in some areas. Community dietary patterns were found to respond directly to improved stock management and food supply,5,6 and multistrategy, community-directed nutrition programs in some remote communities resulted in marked and sustained improvements in anthropometrical, biochemical and haematological risk factors for chronic disease.7,8 Knowledge gained from such studies has broadened the focus of Indigenous nutrition initiatives to include the “supply side” (improving food quality and access to healthy food in remote communities) as well as the “demand side” (promoting nutrition through behaviour change). In 2003, the FoodNorth study provided a comprehensive analysis of remote food supply issues, barriers and leverage points for improvement.9 More recently, the Remote Indigenous Stores and Takeaways Project developed nine practical resources, including a freight-improvement toolkit and a buyer’s guide, to assist remote stores to stock, promote and monitor the sale of healthy food.10 A major barrier is that community stores are seen as small businesses rather than as essential services, like health and education. Encouragingly, several submissions to the recent House of Representatives Inquiry into community stores in remote Indigenous communities detail specific approaches to secure both health and viable business outcomes.11 Remote store groups that combine buying power and operational efficiency (eg, the Arnhem Land Progress Association and the Retail Stores group in Queensland) have shown the benefits of store nutrition policies.9 Outback Stores, a company established by Indigenous Business Australia in 2006, included provision of nutritious food as a key goal, and provides one potential model to support sustainable employment and economic development in independent remote stores.12 The National Aboriginal and Torres Strait Islander Nutrition Strategy and Action Plan 2000–2010 provided a broad framework for nutrition interventions, addressing both supply and demand issues.13 However, implementation of the strategy has neither been sustainably nor well resourced and remains fractured and opportunistic. Therefore, what is still urgently required is systematic, widespread, sustained implementation of evidence-based nutrition interventions. Brimblecombe and O’Dea now rightly highlight the need to also include innovative economic interventions.4 In Northern Territory communities, it has been estimated that up to 36% of the family income is needed to purchase food,14 which is at least double the proportion required by non-Indigenous Australians.15 One of the proposed “Close the Gap” equity targets was that, by 2018, 90% of Indigenous families could access a healthy food basket for under 25% of their income.16 However, nutrition issues were not included in the final National Indigenous Reform Agreement of the Council of Australian Governments. Globally, the dominant economic intervention affecting food pricing is national taxation on food to raise general revenue.17,18 In Australia, the basic foods required to maintain health were mostly exempted from the Goods and Services Tax (GST), and the price of these foods was expected to fall after the introduction of the new tax system in 2000.19 However, in Queensland from 2000 to 2001, the price of a basket of healthy foods increased by 12%, more than twice that of less healthy options.20 This highlights the unpredictability of complex economic systems and the need for rigorous testing of economic solutions to increase access to healthy food.18 Such testing is imperative within remote communities, but baseline data are not readily available as Australia lacks a comprehensive food and nutrition monitoring and surveillance system. It is also crucial that economic interventions support broader models of sustainable development in remote communities. Potential economic instruments include greater differential national taxation on energy-dense, nutrient-poor food (the “fat tax”), and subsidisation of healthy food through freight, in-store pricing and/or direct commodity subvention systems. There is a case for combining both approaches17 to better influence diet among lower socioeconomic groups18 and within relatively closed systems, such as schools and workplaces.17 The provision of free fruit in such settings has also produced sustained benefits in some countries.21 Improving remote area housing to include infrastructure for storage and preparation of food is also vital; in one study, this was serviceable in less than 6% of houses.22 Local food production, including that of traditional foods, may hold promise in some areas. Training and employment of Indigenous nutrition workers23 to deliver services, including budgeting programs like Indigenous FOODcents,24 are also required. Welfare reform and income management programs have great potential in some areas. However, in communities where incomes are quarantined and welfare recipients are required to spend a significant proportion of their income on food and other essentials, good public policy dictates that governments must also ensure that a healthy food supply is actually available and affordable in those communities. For the most vulnerable, food supplementation programs,25,26 if desired and controlled by the community, are warranted. The value of such assistance is greatly increased where food costs are high, and can immediately improve recipients’ dietary quality.19 Within a multistrategy approach, economic interventions tailored to community needs will assist low-income Indigenous Australians in remote communities to obtain the food they need for good health. “Best buys” of such an approach are listed in the Box. Solutions must involve sectors beyond health, including food producers, transporters and retailers, educators, economists and policymakers. “Best buys” to improve Indigenous nutrition and health 1. Continue and expand the reach of successful interventions Increase demand for healthy food Brief nutrition interventions and early interventions in primary care, including “well persons” health checks and follow-up action Prenatal, antenatal and postnatal nutrition programs; culturally appropriate infant growth assessment and action programs; and promoting breastfeeding and appropriate introduction of solid foods27 School-based nutrition-promotion projects, and community food-literacy and budgeting projects Improve supply of healthy food Use of resources developed by the Remote Indigenous Stores and Takeaways Project10 to improve store management practices, and transport and stocking of healthy food Local food gardens and traditional food procurement projects Increase capacity to achieve the interventions given above Train and employ an Indigenous nutrition workforce Improve housing, including food-storage, preparation and cooking facilities Develop a national, coordinated monitoring and surveillance system for food and nutrition 2. Trial economic interventions for widespread roll-out, if successful Food supplementation for women, infants and children Free fruit and vegetables for remote schools and other settings Freight subsidies for getting basic healthy foods to remote areas In-store price “mark-up” of less healthy items, and lower price margins on healthier foods Expansion of the current national differential taxation system to further favour competitive retail pricing of healthy foods

Amanda J Lee PhD, BSc(Nutr), GradDipDiet · Dympna Leonard MPH, BSc(Diet) · Aletia A Moloney MCommNutr · Deanne L Minniecon MHSc(HealthProm)

This position statement was prepared by the Working Group of the Australian and New Zealand Bone and Mineral Society and Osteoporosis Australia. The final statement was endorsed by the Endocrine Society of Australia. Currently, the balance of evidence remains in favour of fracture prevention from combined calcium and vitamin D supplementation in elderly men and women. Adequate vitamin D status is essential for active calcium absorption in the gut and for bone development and remodelling. In adults with a baseline calcium intake of 500–900 mg/day, increasing or supplementing this intake by a further 500–1000 mg/day has a beneficial effect on bone mineral density. Calcium intake significantly above the recommended level is unlikely to achieve additional benefit for bone health.

Kerrie M Sanders GradDipDiet, MHumNutr, PhD · Caryl A Nowson DipNutrDiet, PhD · Mark A Kotowicz MB BS, FRACP · Kathryn Briffa BAppSc(Physio), PhD · Amanda Devine GradDipDiet, PhD · Ian R Reid MB BS, FRACP

To the Editor: Keogh and Clifton’s call for salt reduction in the food supply1 comes when the National Heart Foundation is telling doctors who treat patients with hypertension that they should “recommend low-salt and reduced-salt foods as part of a healthy eating pattern”.2 Humans evolved while eating foods that (with rare exceptions) are low in salt — fresh fruit, vegetables and nuts, supplemented sometimes with fresh meat, poultry or fish — and these foods are still abundant. Using cooking methods that conserve flavour and any of about 300 herbs and spices, they make delicious meals that are low in fat, saturated fat, sugar and salt. Keogh and Clifton’s point is that we need more processed foods that are low in salt. This could be brought about if all doctors prescribed low-salt diets for their patients with hypertension.2 The food industry could hardly fail to respond to an unprecedented demand from the 3.7 million hypertensive Australians who need low-salt foods. Low-salt foods (sodium ≤ 120 mg/100 g) are easy to prescribe, requiring neither a diet nor a dietitian. In Britain, “traffic light” labels identify them at a glance, with green lights for salt. Australian consumers wishing to identify them have to check the mandatory sodium figure in the nutrition information panel provided on all processed food packages for a value of 120 mg/100 g or less. Further information to help consumers identify low-salt foods is available on the SaltMatters website (http://www.saltmatters.org), and a comprehensive handbook for practitioners and motivated patients has also been published.3 A low-salt diet is also particularly important for patients with Ménière’s disorder, because sodium excretion < 50 mmol/day is “more effective and less troublesome than diuretics” for controlling their vertigo.4 This level of sodium excretion occurs when all meals are low in salt.5 The National Heart Foundation’s marginally easier limit of 65 mmol/day allows room for a small mistake or a reduced-salt food, but practitioners must remember that the “combination of diuretic treatment and low dietary salt intake may result in unacceptable volume depletion and hyponatraemia”.6 The National Heart Foundation recommends 24-hour urine sample collections for monitoring dietary compliance (see “Measuring Salt Intake” at the SaltMatters website).

Trevor C Beard

Biting anorexia. A first-hand account of an internal war. Lucy Howard-Taylor. Sydney: Finch Publishing, 2008 (ix + 214 pp). ISBN 9781876 451929. I undertook reviewing this book with some trepidation. I presumed it would be yet another distant “tortured” account of anorexia. I found it quite the opposite. Lucy is an 18-year-old Australian university student. Her depiction of her mental state in anorexia is quite extraordinary. I know that anorexia affects the brain negatively, as a result of both malnutrition and the pervasive thinking disorder. It isn’t until the later chapters that you realise the extreme blunting of her intellect that has occurred. Lucy’s diary is an extraordinarily honest, most intelligent account detailing the process of her illness and pathway towards recovery. I was particularly struck by the difficulties she experienced at all times, and by the depth and sophistication of her thoughts and the enormity of the struggle she went through in attempting to overcome her illness. This book really is the most lucid document and one I have started to recommend to colleagues and to patients. It gave me an insight I had not expected to gain into the extent of the damage done by this illness and the extreme difficulties endured to overcome it.

Simon D Clarke

Available evidence indicates that rates of childhood overweight and obesity have been increasing over the past two decades, but inconsistencies between study methods moderate the strength of this evidence. Concomitant health problems and associated costs make it imperative that primary prevention initiatives are introduced to combat the obesity epidemic. Fundamental to informed action is anthropometric monitoring, which if properly implemented will identify changes over time in specific populations to inform policies, practices and services aimed at prevention and treatment. Sample representativeness is essential for valid trend and prevalence data, but efforts to obtain population-based anthropometric data from school children with the required written parental consent have been thwarted by low participation rates. Notable improvements in participation rates when utilising opt-out consent, in which participation is assumed unless otherwise indicated, are evident from local as well as international studies. Opt-out consent can facilitate anthropometric monitoring, delivering a more informed, best-value-for-money response to the obesity epidemic. Health and education ethics committees need to acknowledge the benefits of opt-out consent for “low-risk” anthropometric measurement, which ultimately upholds the individual’s rights.

Joanne M Stubbs BScPsychol(Hons), MPH · Helen M Achat BEd, MSc, ScD

Overweight and obese patients may develop paradoxical nutritional deficiency from eating high-energy foods with a poor nutrient content. In such patients, this condition is probably under-recognised, and thus untreated. The nutrient density of foods has recently been defined by a score — the naturally nutrient-rich (NNR) score — which assesses the contribution a food makes to the nutrient intake of a 2000 calorie (8360 kJ) daily diet and includes 14 key macronutrients. NNR foods are whole foods that provide the highest nutrient-to-kilojoule ratio. An awareness of the importance of the nutrient density of foods can assist health practitioners to recognise and effectively manage paradoxical nutritional deficiency. Knowledge of the nutrient density of foods helps people wanting to reduce their kilojoule intake to maintain a nutritionally sound diet, providing adequate vitamins, minerals and macronutrients.

Tania P Markovic MB BS, FRACP, PhD · Sharon J Natoli BSc, BND, APD

To the Editor: In addition to its well established link with rickets and osteoporosis, vitamin D deficiency has been associated with increased risk of autoimmune, malignant and cardiovascular disease.1 Marginal deficiency occurs at serum 25-hydroxyvitamin D [25(OH)D] levels of 25–50 nmol/L and frank deficiency at levels < 25 nmol/L,2 but there is some evidence that levels < 80 nmol/L3 or even < 110 nmol/L2 could be suboptimal. In Australia, vitamin D deficiency is most frequent in nursing home residents, dark-skinned veiled women, and residents of southern latitudes.2 However, those who are instructed to habitually minimise sun exposure following a diagnosis of skin cancer may also be at particular risk. We recruited patients with a history of non-melanoma skin cancer, who were not taking vitamin D or calcium supplements, from outpatient dermatology clinics at Royal Prince Alfred Hospital, Sydney (latitude, 33° south). Ethics approval was obtained from the Sydney South West Area Health Service and University of Sydney ethics committees, and all participants provided written informed consent. Serum 25(OH)D levels were measured by radioimmunoassay (DiaSorin, Saluggia, Italy)4 in both late summer (February 2006 or 2007) and late winter (August 2006), with participants completing a 2-week diary detailing daily sun exposure and sunscreen application before each measurement. Twenty-five participants (12 men, 13 women; mean age, 64 years; range, 44–78 years) completed both assessments. We found a significant reduction in mean 25(OH)D levels in winter (summer, 69 ± 3.4 nmol/L; winter, 59 ± 6.2 nmol/L; P < 0.05). In summer, all but one participant had 25(OH)D levels > 50 nmol/L, and eight had levels > 80 nmol/L. In winter, 12 participants had 25(OH)D levels < 50 nmol/L, two had levels < 25 nmol/L, and only three had levels > 80 nmol/L (Box). Hence, using the accepted target value of 50 nmol/L,2 12 participants (48%) were vitamin D-deficient at the end of winter, compared with one (4%) at the end of summer. In summer, the mean reported daily sun exposure was 1 hour (range, 10 min–2.5 h), comprising 40 minutes of off-peak (before 11 am or after 3 pm) and 20 minutes of peak exposure. In winter, the mean daily exposure was also 1 hour (range, 20 min–1.5 h), comprising 30 minutes each of both peak and off-peak sunlight. Volunteers reported wearing sunscreen during about 50% of their summer sun exposure and 27% of their winter sun exposure. Despite mean reported daily sun exposure falling within recommended guidelines, half of our participants were vitamin D-deficient at the end of winter, with almost all demonstrating reductions in winter 25(OH)D levels. Our findings suggest that vitamin D deficiency may be much more prevalent than expected in these patients, and that vitamin D supplementation might be indicated for this group, at least during winter. Vitamin D levels in summer and winter 25(OH)D = 25-hydroxyvitamin D.

Anna-Marie McCombie · Rebecca S Mason · Diona L Damian

Objective: To determine the association, if any, between male-pattern hair loss (baldness) and serum 25-hydroxyvitamin D (25-OHD) levels.Design and participants: A cross-sectional study of 296 healthy middle-aged and older men.Main outcome measures: Degree of baldness was independently assessed by two researchers using the Hamilton–Norwood scale and serum 25-OHD was measured in all men.Results: Classification of the degree of baldness by the two researchers showed a high level of agreement (κ = 0.93). Forty-eight per cent of men had no hair loss or mild frontotemporal recession, 15% had predominant vertex loss, and 37% had significant scalp and vertex loss. After data were adjusted for potential confounding factors — including age, month of 25-OHD measurement, exercise levels, use of sunscreen, skin type and frequency of outdoor hat wearing — no significant differences in 25-OHD levels between these groups was detected (P = 0.60).Conclusions: The degree of baldness does not appear to influence serum 25-OHD levels. The high prevalence of baldness in older men does not explain sex differences in 25-OHD levels. Other novel hypotheses are required to help determine whether baldness serves any physiological purpose.

Mark J Bolland MB ChB, PhD · Ruth W Ames NZCS · Andrew B Grey MD · Anne M Horne MB ChB · Barbara H Mason BSc · Greg D Gamble MSc · Ian R Reid MD