Metabolic diseases

To the Editor: In a recent article that appeared in newspapers such as Melbourne’s The Age and Sydney Morning Herald on 19 Jan 2011,1 one of us (P Z) argued that it is both ineffective and inaccurate to blame those who are overweight and obese for their health problems. It was highlighted that our social, economic, cultural and physical environments are all “obesogenic”,2 acting as barriers to achieving a healthy lifestyle. The article by Proietto in the August 2011 issue of the Journal similarly argued that the obesogenic environment, and its interaction with a person’s genetic make-up, is to blame for the increasing prevalence of overweight and obesity.3 Neglecting to address the role of environmental factors in lifestyle disease may lead to a number of unintended negative consequences. First, healthy eating and being physically active are not easy choices. If attempts are not as successful as first hoped, and if the response from health professionals is simply “try harder”, feelings of guilt and despair can result, which then make it even harder to engage in healthy behaviours. Second, a sole emphasis on individuals’ responsibility for their own health has led governments at all levels in Australia to be passive on this issue. Governments seek to protect us in other ways (eg, legislation to restrict the use and advertising of tobacco), so they now need to be encouraged to take steps towards reducing the obesogenic nature of our environment (eg, introducing policy that ensures affordable and sustainable fruit and vegetable production).4 Finally, focusing on individual health behaviours alone may create or reinforce a social stigma around obesity and related chronic conditions, such as type 2 diabetes.5 When individual behaviour change is the sole focus of prevention and management efforts, the subtext is that the individual is to blame if he or she develops the condition. The astonishing and immediate public response to the aforementioned newspaper article — almost 300 comments were posted online on The Age and Sydney Morning Herald websites alone within hours — reflected an entrenched attitude of blame towards people who are overweight or obese. Given that type 2 diabetes can only be prevented in about 60% of cases,6 these comments reveal and perpetuate a limited understanding of the multiple causes of lifestyle diseases. It remains critical to encourage people to pursue healthy lifestyle choices. However, addressing the obesogenic elements of our environment is just as important. Encouraging patients to become involved in organisations such as The Parents’ Jury, an online network dedicated to improving children’s food and physical activity environments (www.parentsjury.org.au), or to become familiar with community-based initiatives such as Victoria Walks (www.victoriawalks.org.au) may be beneficial. More broadly, it is important for health professionals and their professional bodies to make known to governments their support of policy and other initiatives that make our environ-ment conducive to healthy choices.

Jessica L Browne · Paul Zimmet · Jane Speight

Objective: To define the effectiveness of recent efforts by the Australian Division of World Action on Salt and Health, and the Heart Foundation in New Zealand to reduce sodium levels in breads in Australia and New Zealand.Design and setting: Data on the sodium contents of packaged sliced bread products sold in Australian and New Zealand supermarkets were collected from the product labels of 157 breads in 2007 and 167 breads in 2010, and were compared overall, by bread type, by manufacturer, and between nations.Main outcome measures: Mean sodium values in bread and proportions of breads meeting the targets of 400 mg/100 g in Australia and 450 mg/100 g in New Zealand.Results: Overall mean sodium content in bread in Australia was 434 mg/100 g in 2007 and 435 mg/100 g in 2010; corresponding values for New Zealand were 469 mg/100 g and 439 mg/100 g. The proportion of Australian breads meeting the national target increased from 29% in 2007 to 50% in 2010; the proportion of New Zealand breads meeting the national target increased from 49% in 2007 to 90% in 2010. There were clear differences between the results achieved by different companies.Conclusions: Voluntary efforts by non-governmental organisations have had some impact on sodium levels in bread, particularly in New Zealand. However, substantial room for further improvement remains. If additional reductions are not achieved under the current voluntary arrangements, legislated approaches may be required.

Elizabeth K Dunford MPH · Helen Eyles MSc, PhD · Cliona Ni Mhurchu BSc(Hons), PhD · Jacqui L Webster MA, PhD · Bruce C Neal MB ChB, PhD

Bitôt spots on the temporal limbus of the left eye. Clinical record A 52-year-old man presented to the ophthalmology clinic with a 3-day history of tunnel vision and night blindness (nyctalopia). He reported recently needing to wear a headlamp to see adequately in dim lighting, notably while walking to work early in the morning. The patient had a history of hypertension, hypercholesterol-aemia and osteoporosis. Twice in the previous 2 years, he had seen a neurologist for symptoms of lower limb paraesthesiae. At that time, peripheral nerve conduction studies gave normal results, and a clinical diagnosis of peripheral neuropathy secondary to vitamin B12 deficiency was made. Supplement-ation with vitamin B12 and folate was initiated. He also described a 3-hour episode of tunnel vision 2 years before presentation. Examination revealed an otherwise well man with a body mass index of 27 kg/m2 (ie, in the overweight range). His best corrected visual acuity was 6/18 in the right eye and 6/9 in the left eye. Anterior segment examination revealed Bitôt spots, and no staining of the cornea with fluorescein (Figure). Pupillary examination revealed a relative afferent pupillary defect of the right eye, grade 1/4, indicating optic nerve dysfunction. Ocular motility and intraocular pressures were normal. Fundoscopy showed normal peripheral retinal pigment epithelium, and normal discs and maculae. Humphrey visual field 30-2 testing showed peripheral field constriction. Results of the Farnsworth–Munsell D-15 hue test for colour vision were normal. Dark-adapted electroretinography (ERG) revealed bilaterally decreased amplit-udes, consistent with diminished rod function. The results of computed tomography and magnetic resonance imaging of the brain and orbits, using contrast, were normal. Investigations revealed a markedly reduced vitamin A level (0.1 μmol/L [reference range, 1.4–4.0 μmol/L]). Results of a full blood count, electrolyte levels, and liver and thyroid function tests were normal. Vitamin B12 and folate levels were high, consistent with supplementation. Normal results of a malabsorption screen, including levels of fat-soluble vitamins D, E and K, were obtained, and test results for parietal cell and intrinsic factor antibodies were negative. Test results for antiendomysial antibodies were also negative, as were those for IgA and IgG antigliadin antibodies, thus excluding coeliac disease. A diagnosis of xerophthalmia (dryness of the conjunctiva and cornea) was made on the basis of the symptoms of nyctalopia and tunnel vision, as well as the findings of bilateral Bitôt spots, hypovitaminosis A, and diminished rod function on ERG. A dietary history revealed that the patient had suffered from self-diagnosed food intolerance for most of his life. Since childhood, his diet had consisted exclusively of potatoes, white bread (but he refused to eat butter and margarine) and cola. He described nausea and vomiting after eating any other foods. The patient underwent multidisciplinary evaluation by a neurologist, gastroenterologist, psychiatrist, dietitian and psychologist. Dietary supplements were prescribed and cognitive behaviour therapy was initiated. The patient was treated with 100 000 IU of vitamin A daily, given orally for 3 days, followed by 50 000 IU for 14 days. Humphrey visual field results and visual acuity improved within 3 days of commencing treatment. After a month, visual acuity had improved to 6/6 in both eyes, and the Bitôt spots had completely resolved. The relative afferent pupillary defect was no longer present, and Humphrey visual field and ERG results had returned to normal. Vitamin A deficiency is a systemic illness which can increase an individual’s risk of blindness, severe infections and mortality.1 It is rare in developed countries like Australia.2 Vitamin A deficiency and xerophthalmia in developed countries are reported in patients with malabsorption syndromes or liver disease, in those who have had major gastrointestinal surgery, in people with alcoholism, and in those with anorexia nervosa and other psychiatric disorders.3-6 This case is unique because our patient did not have any of these risk factors. This case also highlights the importance of clinicians regularly taking a thorough dietary history, especially in the context of other indications of nutritional insufficiencies, such as osteoporosis and previous vitamin B12 deficiency. Vitamin A is a fat-soluble vitamin found as retinol in dairy products and as provitamin A carotenoids in some fruits and green leafy vegetables.1,7-9 The first clinical evidence of vitamin A deficiency often occurs in the visual system and produces xerophthalmia. The ocular changes of xerophthalmia generally occur in a predictable pattern, as described by the World Health Organization.1 The first stage of xerophthalmia is nyctalopia, the result of defective regeneration of retinal rhodopsin.3,7-9 This responds rapidly to vitamin A therapy, and patients often report regaining their scotopic vision (vision under low-light conditions) within 24–48 hours after the initiation of treatment.1,3,7,9 The second stage of xerophthalmia is conjunctival xerosis, or drying, in which loss of goblet cells and squamous metaplasia of the conjunctiva occur.1,3,7,8 Bitôt spots are bilateral triangular patches of keratinised epithelium at the temporal limbus and nasal limbus of the eye.1,3,7 Colonisation of these patches by saprophytic bacilli, including Corynebacterium xerosis, results in a foamy appearance.1,3,8 Conjunctival xerosis and Bitôt spots respond to vitamin A therapy in 1–5 days.1,3 Corneal xerosis occurs primarily because of instability of the tear film as goblet cells are lost, with subsequent keratinising metaplasia of the ocular surface.1,8 Corneal xerosis usually responds to vitamin A therapy in 1–2 weeks.1,9 If left untreated, corneal drying can result in ulceration, with subsequent scarring and keratomalacia.2,3,7,8 Keratomalacia is a rapidly progressive and irreversible liquefactive necrosis of the cornea that can ultimately lead to perforation and spontaneous loss of intraocular contents.1,3,9 Lessons from practice Vitamin A deficiency is rare in developed countries like Australia. Visual symptoms can often be the first manifestation of a systemic illness, such as vitamin A deficiency. A thorough nutritional screen, including a dietary history, is essential, especially in the context of any other nutritional deficiency. Early diagnosis and treatment of vitamin A deficiency can be curative, preserving vision and life. Uncommonly, in vitamin A deficiency, the xerophthalmic fundus exhibits yellow and white dots peripherally, sometimes associated with a corresponding scotoma (area of diminished vision).1,7-10 These changes respond well to treatment, often returning to normal within 2–4 months.1,8,9 The diagnosis of vitamin A deficiency is made by a directed history and clinical findings, and confirmed by the presence of a low serum vitamin A level, and an abnormal electroretinography result.3,9 In our case, the diagnosis was made accordingly, and all the pathological findings resolved with vitamin A therapy. Vitamin A deficiency is usually treated by administering 200 000 IU of vitamin A orally on two successive days, followed by an additional dose 1–4 weeks later.1 Administration of intramuscular vitamin A is reserved for patients with malabsorption, or those who are unable to tolerate medications orally.1 Ocular vitamin A has not been shown to be beneficial because of the systemic nature of vitamin A deficiency.7 In summary, we present a unique case of vitamin A deficiency and xerophthalmia in an unlikely candidate for malnutrition. Hypovitaminosis A can have potentially devastating visual and systemic effects. To prevent this happening, it is important to maintain a high degree of suspicion, especially in the context of other nutritional deficiencies.

Esra Sanli MB BS, BMedSc · Edwin C Figueira MB BS, MSc, MS(Ophth) · Gaurav Bhardwaj MB BS · Stephanie L Watson MB BS, FRANZCO, PhD · Ian C Francis FRACS, FASOPRS, PhD

How can implementing a population-wide salt-reduction program be so hard? For most of human evolution, the average daily diet contained a fraction of a gram of salt and our physiology developed accordingly.1 A few thousand years ago, with the discovery that salt could preserve food, average intake started to rise. Now, with salt poured into the food supply, average Australian consumption levels are many times our physiological need.2 Populations eating the level of salt upon which we evolved are now few, but they provide a window into normal physiological processes. One of the most notable findings is that their blood pressure levels do not rise with age.3 Despite recent highly publicised reports,4 there is little debate about the adverse impact of salt on human health.5 The totality of the evidence is convincing and the unbiased findings from randomised trials of salt reduction particularly so. While a number of non-randomised studies have suggested health benefits of salt consumption,4 the publicity they receive greatly exceeds their real significance. Observational nutritional epidemiology is incredibly difficult to do well, and the diversity of findings almost certainly reflects methodological challenges, not discrepant science. Although direct evidence from a single adequately powered mortality and morbidity trial of salt reduction is lacking, the circumstantial evidence remains striking and the likelihood that reduction in salt intake will not reduce vascular risk is small. The strength of the evidence base has persuaded multiple national and international organisations of the need to reduce salt consumption.5 All hypertension guidelines advocate consuming less salt,6 and more than 30 countries now have some form of population-based salt-reduction program in place.7 A series of influential reports has highlighted the large health gains that might be achieved from such national programs and the low costs required to deliver them.8 The issue is no longer whether salt reduction should be a goal, but how it can be achieved. The reason salt reduction presents such a great public health opportunity is that almost everyone eats far more than they need. Average consumption in Australia is between 8 and 10 grams per day,1 with immediate and long-term implications for blood pressure. The early effects occur within weeks and the chronic effects over decades. As shown by Huggins and colleagues in this issue of the Journal,9 and previously noted by the Intersalt study,10 a daily intake 6 grams above physiological need will push up systolic blood pressure by a few millimetres of mercury in the short term and thereafter by about half a millimetre each year. This chronic effect translates into 25 mmHg over 50 years, with enormous implications for individual and population risks of vascular disease. Blood pressure is a leading cause of disease burden in Australia,11 and our strategy for preventing disease attributable to high blood pressure is hypertension control — individuals are diagnosed as hypertensive and treated within the medical system. Hypertension is currently the most frequent reason for a primary care consultation, with annual direct health care costs of more than a billion dollars.12 For those who need and receive it, antihypertensive therapy is a highly effective intervention. Unfortunately, the clinical approach also has some limitations. First and foremost among these is that half of all disease caused by high blood pressure occurs among people without hypertension.13 Risks start to accrue well below the blood pressure level of 140/90 mmHg that generally defines hypertension, and systolic blood pressure levels of 125–135 mmHg are associated with greater risks than a level of 120 mmHg. While more moderate than the risks faced by those with hypertension, these blood pressure levels cause a very large number of adverse events because these are the blood pressure levels of most of the population. The limited coverage achieved by the clinical hypertension control strategy further reduces its effectiveness. Only about half of hypertensive people are identified and treated;14 less than half of these get to target blood pressure levels,14 and almost none achieve a systolic pressure of 120 mmHg or below. Accordingly, clinical management of hypertension in Australia probably prevents only about a 10th of all blood pressure-related disease. A plausible population-wide salt-reduction program that removed salt at the source could within a few years avert a similar proportion of disease burden at an annual cost of just $10–20 million.5 To achieve this, the Australian Government simply needs to set and enforce salt targets for foods, as has been done in the United Kingdom.7 Average salt consumption would fall, mean population blood pressure would immediately follow, and the long-term rise in blood pressure with age would be attenuated. The real question is how this can be so hard. For almost no extra cost and at no risk, there is a high likelihood we could double the proportion of blood pressure-related disease averted within just a few years. With a proven overseas model to follow,7 our failure to take the action required is bordering on negligent. No one is going to lose their parliamentary seat and no one is going to go out of business if they make this happen. There are just going to be a lot of unnecessary strokes and heart attacks while the people pickling us figure this out.

Bruce C Neal MB ChB, PhD, FRCP

Objective: To assess the relationship between dietary sodium intake, as measured by urinary electrolyte excretion, and blood pressure within a population of older Australian adults.Design, setting and participants: A cross-sectional study of adults enrolled in the Melbourne Collaborative Cohort Study, stratified by sex, country of birth (Italy, Greece, Australia/New Zealand) and age (50–59 and 60–75 years). Blood pressure measurements were taken in 2003–2007 and 24-hour urine collections in 2007–2008.Main outcome measures: 24-hour urinary excretion of sodium and potassium, urinary sodium-to-potassium ratio, and clinic blood pressure measurement.Results: The mean ± SD age of 783 participants was 64.0 ± 6.3 years. Mean ± SD urinary sodium was 155.1 ± 63.1 mmol/day (8.9 ± 3.6 g salt/day), urinary potassium was 82.3 ± 27.9 mmol/day, and urinary sodium-to-potassium ratio was 1.99 ± 0.83. In the 587 participants with blood pressure measurements, urinary sodium and the sodium-to-potassium ratio were both associated with systolic blood pressure in all adjusted and unadjusted models (mmHg change per 100 mmol/day increase in sodium: regression coefficient, 2.3, 95% CI, 0.1–4.6; P = 0.049, adjusted for age, sex, body mass index, country of birth and antihypertensive medication use).Conclusion: This study has demonstrated, for the first time within an Australian population sample of older adults, that sodium intake is positively associated with blood pressure. These results suggest that a population-wide reduction in sodium intake could be effective in reducing blood pressure in adults in Australia.

Catherine E Huggins BSc(Hons), PhD · Sharleen O’Reilly BSc(Hons), PhD, CertHEd · Maree Brinkman BSc(Nutrition), MND · Allison Hodge BSc, GradDipDiet, PhD · Graham G Giles BSc, MSc, PhD · Dallas R English BSC, PhD · Caryl A Nowson PhD, DipNutDiet

There is little evidence that public health measures adopted so far have had any impact on the rise in the prevalence of obesity. Weight-loss programs have a very high long-term failure rate. There is emerging evidence that weight is regulated by the hypothalamus and is physiologically defended. There is also a strong genetic predisposition to the development of obesity. The availability and promotion of high-energy foods and the absence of any obligatory need for physical activity compound the problem, but this social change is not easily reversible. One way forward is to focus public health measures on preventing obesity in children while making resources available to treat people who are already obese, including providing funding for bariatric surgery in public hospitals.

Joseph Proietto MB BS, FRACP, PhD

A 27-year-old woman was being treated with gastrojejunostomy feeding for severe anorexia nervosa. The position of the gastrojejunostomy tube was checked by fluoroscopy on the day of insertion (Figure, A, arrow). The next day, the patient presented with abdominal pain and “shortening” of the external portion of the tube. Repeat fluoroscopy showed migration of the tube (Figure, B, arrow). Computed tomography showed two segments of jejunojejunal intussusception (Figure, C, arrow and inset, and D, straight arrow) centred around the tube (Figure, D, curved arrow), with an intervening segment of normal jejunum (Figure, D, label J). The patient’s gastrointestinal tract was intact. The intussusceptions were reduced by applying traction on the tube under fluoroscopic guidance, and the patient resumed tube feeding without recurrence.

Uei Pua

Objective: To assess the impact of the quick-service restaurant industry (QSRI) self-regulatory initiative on fast-food advertising to children on Australian commercial television.Design and setting: Analysis of advertisements for foods on the three main free-to-air commercial television channels (channels 7, 9 and 10) in Sydney, Australia, over 4 days in both May 2009 and April 2010 in terms of: number of advertisements; types of food (coded core [healthy] foods, non-core [unhealthy] foods, miscellaneous foods; or fast foods); whether advertised meals were intended for children; whether advertisements were broadcast during children’s peak viewing times; and whether the company in question was a signatory to the QSRI initiative.Main outcome measures: Change in the mean frequency and rate of food advertisements per hour from 2009 to 2010; change in the types of fast-food meals (healthier alternatives [at least one nutrient-dense, low-energy food considered part of a healthy diet for children], non-core [high in undesirable nutrients and not considered part of a healthy diet for children], and other) being advertised; and proportion of children’s energy requirements provided by fast-food meals.Results: From 2009 to 2010, the mean frequency of fast-food advertisements increased from 1.1 to 1.5 per hour. While non-core fast foods comprised a lesser share of fast-food advertising in 2010 than 2009, the mean frequency at which they were advertised during times when the largest numbers of children were watching television remained the same (1.3 per hour in both 2009 and 2010). Family meals advertised for children’s consumption in 2010 provided energy far in excess of children’s requirements.Conclusions: Children’s exposure to unhealthy fast-food advertising has not changed following the introduction of self-regulation, and some fast foods advertised for children’s consumption contain excessive energy. The limited impact of self-regulation suggests that governments should define the policy framework for regulating fast-food advertising to children.

Lana A Hebden BND · Lesley King MPsych(Hons) · Anne Grunseit PhD · Bridget Kelly MPH, BSc(Nutr)(Hons) · Kathy Chapman MNutrDiet, BSc

To the Editor: Weight fluctuations may lead to significant changes in a patient’s treatment, so it is vital that hospital scales are accurate. A literature review revealed that calibration,1 accuracy2 and centralised hospital quality control3 of hospital scales were issues that are being recognised and addressed around the world. We audited all scales at the Royal Melbourne Hospital, city campus, to assess their accuracy and identify the types of scales that are likely to be most accurate. A preliminary survey identified all scales on the wards and in outpatient departments. On a single survey day, each scale was categorised and photographed. Scales were “zeroed” and standard weights of 5 kg, 10 kg, 15 kg and 20 kg, and a person whose weight had been established elsewhere as 106 kg, were then weighed on each scale. Our primary measure of accuracy was the difference between 106 kg and the recorded weight of the person, as this most closely approximated the weight of an average patient (rather than using the 5, 10, 15 and 20 kg weights). Forty-three of 50 scales identified in the hospital were tested. Scales that were excluded were either not working or not able to be tested with the weights we used. All scales in the outpatients department were digital (22). On the wards, there was a mix of sit-on (6) and stand-on (15), and digital (9) and analogue (12) scales. The digital scales had an accuracy (range around the standard weight) of − 1 kg to +1.5 kg, compared with an accuracy of − 3.5 kg to +1 kg for the analogue scales (P = 0.006; Wilcoxon signed rank test). Interquartile ranges were − 0.45 kg to +0.07 kg for digital scales and − 2 kg to +0.5 kg for analogue scales. The mean deviation from the correct weight was 0.06 kg for digital scales and 0.55 kg for analog scales. The most accurate scales were in the renal wards, used by dialysis outpatients and inpatients. Some areas had scales that were unusable by patients, such as sit-on scales in the geriatric ward (Box 1) that were difficult to mount. A haematology ward, where decisions are often made on the basis of changes in weight, had five sets of scales, with significant inaccuracies and differences between them. In one ward, no scales could be located, and five out of 23 outpatient rooms had no scales. The digital scales were more accurate than the analogue scales (Box 2). In areas where treatment decisions are made on the basis of changes in weight, scales should regularly be checked for accuracy, and patients should be weighed on the same scales each time they are weighed. For greater accuracy and consistency in measuring patient weights, we recommend that all scales be upgraded to digital scales throughout the hospital. 1 Sit-on analogue scale at Royal Melbourne Hospital, unusable for some patients 2 Weight variations in 43 digital and analogue scales at Royal Melbourne Hospital * As measured using standard weights of 5 kg, 10 kg, 15 kg, 20 kg and a 106 kg person.

Rimma Goldberg · Geoffrey Hebbard

To the Editor: We read with interest the recent letter by He and colleagues.1 The authors described a case of ischaemic stroke in a patient with scurvy and considered whether there was a connection between the two conditions. They referred to evidence that vitamin C deficiency may be a risk factor for cerebrovascular disease, but acknowledged that a direct causal link is unlikely to be established. We propose adiponectin as the causal link between vitamin C deficiency and stroke. Adiponectin is an adipokine, secreted in multimers by adipose tissue, with insulin-sensitising, antiatherogenic and cardioprotective properties.2 A decrease in adiponectin levels — particularly the more biologically active, high molecular weight (HMW) multimers — is implicated in a number of disease states, such as obesity, type 2 diabetes, heart disease and some cancers. Adiponectin has also been reported to have cerebroprotective properties,3 and there is some evidence that levels may be reduced in patients with cerebrovascular disease.4 A recent study demonstrated that vitamin C supplementation increases the proportion of HMW adiponectin secreted from human adipocytes.5 Vitamin C levels are lower in obese and diabetic patients, and the patient reported by He et al had also been recently diagnosed with type 2 diabetes. While scurvy is admittedly rare, He and colleagues noted that subclinical vitamin C deficiency is not uncommon in the general population (about 10%). We suggest that it would be worthwhile to assay plasma vitamin C levels and total and HMW adiponectin levels in patients presenting with cerebrovascular events, and to undertake prospective studies to determine whether vitamin C supplementation improves patients’ adiponectin levels. Increased HMW adiponectin levels could be explained, at least in part, by the role of vitamin C in the multimerisation of adiponectin. Adiponectin levels are also reduced in other vascular conditions, such as ischaemic heart disease and peripheral vascular disease.4 As plasma vitamin C levels of patients with these diseases are also reduced, it is tempting to posit that vitamin C supplementation could have a role as a treatment, or even a prophylactic, in populations at risk of a range of adiponectin-related vascular diseases.

Felicity J Rose · Jonathan P Whitehead

From public health pariah to pin-up bunny? Chocolate manufacturers around the world know that the Easter bunny (EB) is highly effective at enticing us to eat chocolate. Up to 28% of one manufacturer’s yearly chocolate sales occur in the lead up to Easter.1 Another company produces about 500 million of one particular Easter egg variety — the United Kingdom’s most sold Easter confectionery.2 The EB has been popularised and exploited by chocolate manufacturers and other companies selling this energy-dense, nutrient-poor (EDNP) food. Since when did bunnies lay eggs made of chocolate? Is this a conspiracy to sell lucrative chocolate eggs? I have argued that Santa Claus is a public health pariah who advertises unhealthy products to children and normalises obesity,3 but what about the EB — is this bunny an innocent fairytale character4 or another unhealthy childhood role model? Eggs, rabbits, Easter and chocolateFor millennia, eggs were gifts to celebrate the coming of spring, while rabbits and hares represented fertility and new life after winter.5 With the commercialisation of Easter in the 20th century, chocolate Easter eggs grew in popularity and, through some excellent marketing, chocolate manufacturers bred a chocolate-egg-bearing rabbit. Then, in a move that would have made Willy Wonka proud, they made Easter bunnies of chocolate (Box 1) and sold both the bunny and the eggs!5 EDNP foods, obesity and chronic diseaseAlthough the EB’s delivery practices may provide a better role model than Santa’s, with its vigorous round-the-world hopping sustained only by carrots, the EB may have a more direct impact on obesity by promoting and distributing EDNP food. Excess chocolate has been linked to dental caries and obesity, and obesity has been linked to a significantly higher risk of type 2 diabetes,6,7 hypertension,8 gall bladder disease,9 liver disease,10 and heart disease and stroke,11 and to a small increased risk of cancer (breast, colorectal and endometrial cancers).12,13 Chocoholics and EDNP food companies quote studies showing that cocoa polyphenols protect against cardiovascular disease (CVD).14 However, such studies do not adequately account for confounders, such as comorbidities, or the effect on those with existing CVD who are advised to avoid EDNP food. Also ignored is the fact that most Easter eggs have only a small proportion of cocoa solids and high levels of hydrogenated vegetable oil (trans fats). The negative health effects of chocolate are minimal when it is consumed sensibly, but at Easter this seems to be rare.1,2 Marketing, exploitation, children and advertisingIn the same way that Santa was a feature of Coca-Cola advertising,15 the EB’s role is to sell chocolate eggs to children. This is not the first time that iconic childhood figures have been used successfully to market products to children and create associations between a product and happy times.16,17 Fictional characters such as Ronald McDonald have become more familiar to children in the United States than the American President or the Pope.17 International reviews have found that heavy marketing of EDNP food, high in salt, sugar and fat, is likely to have deleterious effects on children’s diet.18 According to the World Health Organization, such advertising contributes to children being overweight and obese and is an important area for preventive action.19 Given that the EB’s marketing may influence hundreds of millions of children, chocolate intake only needs to increase in one in 10 000 children to have a deleterious effect on the health of millions of children. In Australia, the National Preventative Health Taskforce recommends phasing out “premium offers, toys, competitions and the use of promotional characters, including celebrities and cartoon characters, used to market EDNP food and beverages to children”.13 Similar regulation is occurring in the UK, the US, Canada, Norway and Sweden.20-22 In Sweden and Norway and the Canadian province of Quebec, there are extensive legislative prohibitions on advertising to children. These commercial advertising laws might mean the end of the EB in advertising; after all, wherever the EB hops, it is advertising to children. As a “promotional character”, will the EB be phased out in Australia? Adults, childhood memories and learned behaviourSome ground-breaking research has shown that belief in the EB decreases with age,4 but the public health implications do not — much of the chocolate consumed at Easter is in fact consumed by adults.23 Having been conditioned as children to associate the EB and chocolate with happy memories of Easter, adults (over)consume chocolate at Easter as they relive these happy feelings and memories. Conceivably, the positive psychological effects of low doses of Easter chocolate consumption might outweigh the negative ill health effects, but at higher doses of sugar and fat, the marginal benefit decreases and is eventually negated. The EB promotes high-dose chocolate overindulgence by children at Easter, a habit which then becomes normalised behaviour for many adults. Easter egg hunts, violence, injury and chokingAt Easter, egg hunts are common, as children search for eggs hidden by the EB. Conceivably, these might encourage healthy physical activity: children can run very fast when chocolate Easter eggs are awaiting discovery. Simple modelling, however, debunks this theory (Box 2). Assuming the average child finds, and then consumes, fourteen 10 g eggs and one 125 g egg (5819.9 kJ), a basic energy expenditure formula suggests that a 338-minute (5.6-hour) Easter egg hunt is required to burn off the kilojoules gained from the eggs consumed.25 Not only do Easter egg hunts promote an unhealthy energy balance, they may also contribute to the burden of injury in children (with injury being the most significant cause of mortality in 1–18-year-olds).26 Given that sharing chocolate eggs is not instinctive for young children, Easter egg hunts have the potential to cause emotional distress and interpersonal violence. We have probably all witnessed, or been involved in, a fight over the EB’s treats. Furthermore, the stimulant effect of the caffeine and theobromine compounds in chocolate may accentuate this risk. Admittedly, children taking part in Easter egg hunts do not normally sustain serious injury, but, as eminent epidemiologist Geoffrey Rose detailed in his seminal work The strategy of preventive medicine, when a rare risk is widespread, the impact can be large.27 For example, suppose that the Easter egg hunt injury rate is one in 10 000 participating children (ie, a very low risk); if, on Easter Sunday in the US, 30 million children participate in hunts, then more than 3000 children would be injured! Another danger is choking. One could scarcely design a more perfect choking hazard: small, colourful, foil-wrapped chocolates marketed specifically to our most vulnerable consumers (Box 3). Given the EB’s potential to promote this kind of injurious behaviour, I consulted surveillance sources for injuries related to “Easter bunny” or “Easter eggs”. The codes in the Victorian Emergency Minimum Dataset related to choking are: “Foreign object obstructing airway” (W44) and “Inhalation and ingestion of food causing obstruction of respiratory tract” (W79),28 but there is no category permitting analysis of choking related to Easter eggs. Perhaps W79 should be further differentiated into “Inhalation and ingestion of Easter egg causing obstruction of respiratory tract”. Easter, chocolate and international public healthThe EB, like Santa, has an international profile as an export item to the developing world. The potential for the EB to be misused may be even greater in countries where advertising is less regulated. For example, Easter is celebrated in countries such as India, where Good Friday and Easter Monday are national holidays.29 Just as Coca-Cola and Santa have colonised the developing world, the EB is sure to follow. How can we make the EB the pin-up bunny of public health?Although bordering on the ridiculous, my article highlights the fact that, due to its popular acclaim, the EB, like Santa, can be used to promote unhealthy behaviour. Giant multinational food and beverage companies realised long ago that celebrities, like the EB, sell commodities, including unhealthy ones, and children are a particular target. We could change this by: Minimising the harmful effectsEducating parents to protect their children from the deleterious effects of belief in the EB. Ferreting out the EB is not the “nanny state” imposing health behaviour on our community; it is protecting children from “nanny parents” imposing an unhealthy EB belief on their children.4 Children are generally very happy with themselves for having worked out that their parents are deluded in this belief. They always knew Easter was all about chocolate and not the EB anyway. Instituting better surveillance so we can measure the EB’s impact on public health (eg, include “EB-related deaths” in the WHO’s standardised documentation).30 Restraining EDNP companies from employing the EB as their chief marketing consultant to sell unhealthy food to children, perhaps through employment conditions such as a levy on the EB’s advertising activities (consistent with the recently recommended levy on advertising of EDNP food and alcohol31). Changing the EB’s imageGiven the EB’s potential for good, it could become a public health pin-up bunny, supporting campaigns that encourage children to eat the recommended daily five servings of vegetables and two servings of fruit. Chocolate egg hunts could become brussels sprout hunts! After all, the EB itself would advocate for this change, given that bunnies do not digest chocolate particularly well. 1 Would you trust this bunny? 2 Easter egg hunts — hunting time needed to burn off chocolate eggs consumed No. of 10 g Easter eggs Chocolate (g) Energy (kJ) consumed Running time required (min) 5 50 1098.3 63 10* 100 2196.6 127 15 150 3294.9 190 20 200 4393.2 255 25 250 5491.5 318 30 300 6589.8 381 * The average Australian consumes 10 Easter eggs.24 3 A perfect choking hazard

Nathan J Grills DPhil(Oxon), MPH, MB BS

To the Editor: Van Der Weyden states that “obesity” has negative connotations and the capacity to stigmatise.1 “Intending to give minimal offence and shifting the focus from the person to the condition”, people substitute politically correct terms.1 Medical practice should be scientifically, rather than politically, correct. Language aside, obesity is a blind spot in clinical practice because of the lack of any useful and accurate measure to categorise the condition. Body mass index (BMI) is the universal standard, but it is a very flawed measure. The results of epidemiological studies that support its use depend on huge population numbers, ethnic homogeneity and the exclusion of confounders including smoking and coexisting chronic disease. There is an absence of any epidemiological data showing that reducing overweight or obesity improves outcomes, despite them being frequently cited as risk factors. However, bariatric surgery has been shown to reduce cardiovascular disease, diabetes and cancer incidence.2 Central obesity is a much more powerful predictor of total mortality and cardiovascular disease mortality than BMI.3 In particular, the waist-to-hip ratio (WHR) is useful in population studies, showing precision and a lack of bias over a wide range of ethnic groups.4 Waist circumference is a better predictor than BMI but, like BMI, requires ethnic-specific criteria and is difficult to implement in today’s multiracial societies. WHR performs better as a predictor of cardiovascular disease than all lipid fractions, including total cholesterol and low-density lipoprotein cholesterol.3,5 Lowering lipid levels by drug therapy in the clinical trial setting reduces cardiovascular end points by 20% to 25%. In this context it is pertinent to note that the cost of subsidising prescriptions for lipid-lowering drugs in the financial year 2009–10 was almost $1.5 billion.6 In contrast, there is no simple prescription available to reduce levels of obesity. Healthy eating will always be important. And to make an impact on obesity, 60–90 minutes of moderate physical activity daily is required,7 but the importance of exercise is constantly overlooked and underprescribed. Studies in the United States show that physical activity, recorded daily, reduces cardiovascular disease mortality by about 37%–53%.8 Japan has undertaken an ambitious campaign to identify and counsel employees with excessive waistlines.9 This initiative will be followed with interest. A public health focus on early identification and prevention of central obesity is therefore at least as important in reducing cardiovascular disease mortality as is the measurement and treatment of lipids and hypertension. People with central or abdominal obesity have a serious health hazard and should be informed. “Political correctness” describes a practice that avoids giving offence to minorities. In view of the current epidemic of obesity, the language that we use should be explicit.

Timothy A Welborn · Satvinder S Dhaliwal

Objective: To test the hypothesis that lower 25-hydroxyvitamin D (25[OH]D) levels in late pregnancy are associated with poorer glucose control in gestational diabetes mellitus (GDM).Design and setting: Retrospective cross-sectional study, in a GDM clinic at a tertiary referral centre.Patients: Women attending the GDM clinic at Westmead Hospital from 1 February 2007 to 1 February 2008, excluding those with prepregnancy glucose intolerance.Main outcome measures: Levels of glycated haemoglobin (HbA1c) and 25(OH)D measured during the third trimester; maternal age, ethnicity, body mass index (BMI) and occupational status; and results of oral glucose tolerance testing (OGTT).Results: 147 women with a mean gestational age of 35 ± 2 weeks were included, of whom 41% had insufficient or deficient levels of 25(OH)D (≤ 50 nmol/L). Ethnicity, occupational status and season significantly influenced 25(OH)D levels (P < 0.01 for all) but BMI did not. 25(OH)D levels were inversely associated with fasting and 2-hour blood glucose levels during OGTT (Spearman r = − 0.16; P = 0.05 for both) and with log[HbA1c] (Spearman r = − 0.32; P < 0.001). BMI and insulin doses were also associated with HbA1c levels. Multivariable analysis identified 25(OH)D and blood glucose levels during the OGTT as independent predictors of HbA1c levels.Conclusions: Lower 25(OH)D levels are independently associated with poorer glycaemic control. Future randomised trials are needed to determine whether vitamin D plays a role in glycaemic control in GDM. Regardless, maternal vitamin D insufficiency has adverse effects including neonatal hypocalcaemia and rickets. The 41% prevalence of inadequate 25(OH)D levels in the women in our study is unacceptably high. We propose routine 25(OH)D testing of all pregnant women at screening for GDM or earlier, and treatment of women who are found to be deficient.

Sue Lynn Lau MB BS, FRACP · Jenny E Gunton MB BS, FRACP, PhD · Neil P Athayde MB BS(Hons), FRANZCOG, CMFM · Karen Byth PhD · N Wah Cheung MB BS, FRACP, PhD

Objective: To examine the feasibility of balancing sunlight exposure to meet vitamin D requirements with sun protection guidelines.Design and setting: We used standard erythemal dose and Ultraviolet Index (UVI) data for 1 June 1996 to 30 December 2005 for seven Australian cities to estimate duration of sun exposure required for fair-skinned individuals to synthesise 1000 IU (25 μg) of vitamin D, with 11% and 17% body exposure, for each season and hour of the day. Periods were classified according to whether the UVI was < 3 or ≥ 3 (when sun protection measures are recommended), and whether required duration of exposure was ≤ 30 min, 31–60 min, or > 60 min.Main outcome measure: Duration of sunlight exposure required to achieve 1000 IU of vitamin D synthesis.Results: Duration of sunlight exposure required to synthesise 1000 IU of vitamin D varied by time of day, season and city. Although peak UVI periods are typically promoted as between 10 am and 3 pm, UVI was often ≥ 3 before 10 am or after 3 pm. When the UVI was < 3, there were few opportunities to synthesise 1000 IU of vitamin D within 30 min, with either 11% or 17% body exposure.Conclusion: There is a delicate line between balancing the beneficial effects of sunlight exposure while avoiding its damaging effects. Physiological and geographical factors may reduce vitamin D synthesis, and supplementation may be necessary to achieve adequate vitamin D status for individuals at risk of deficiency.

Kellie L Stalgis-Bilinski BSc, MNutrDiet, APD · John Boyages MB BS(Hons), FRACR, PhD · Elizabeth L Salisbury MB BS(Hons), FRCPA, FFOP · Colin R Dunstan PhD(Med), MSc, BSc(Hons) · Stuart I Henderson BSc, PhD(Applied Physics) · Peter L Talbot BSc, PostgradDipNutrDiet, MSc

Rosemary Stanton believes that the Heart Foundation Tick program misguides consumers YES The National Heart Foundation of Australia plays a valuable role in bringing heart disease to public attention. However, shortcomings of their Heart Foundation Tick program1 demand caution. Media releases proclaim that the Tick has been “awarded to” or “earned by” particular foods. These must meet the Heart Foundation’s nutritional criteria, but companies then pay to use the Tick. For food companies, whose purpose is to make a profit, the Tick is a marketing exercise. By tweaking products (where necessary) and paying for the Tick, companies gain credibility by linking their brand to the positive emotions attached to the Heart Foundation. The extra cost is passed on to the shopper. Effects on food pricesThe cost of food is a particular concern for people on low incomes, who have a higher incidence of diet-related health problems.2 Processed foods that bear the Tick almost invariably have a higher price, while cheaper products in many food categories may have a nutritional profile at least as good as those with the Tick — sometimes better. Rolled oats with the Tick are 4.5 times the price of house-brand oats. How can this be justified? A similarly expensive Tick approved product dilutes rolled oats with 20% wheat starch, adding inulin for extra fibre. Why? Tick criteriaThe Heart Foundation’s criteria for “earning” the Tick are a cause for concern, especially the variation in its criteria for different product types. To earn the Tick, tomato sauce must have no added salt, but a similar restriction does not apply to salad dressings. Some salad dressings with the Tick contain more than 600 mg sodium per 100 mL. A much healthier option is homemade dressing, such as olive oil with lemon juice or vinegar — quick and easy to make, with virtually no sodium. In food categories such as pies, frozen pizza, fast foods, sweet biscuits, rolled fruit confectionery and frozen meals, products with the Tick may represent a slight improvement on similar products, but these food types do not deserve any stamp of credibility. The appropriate message for an overweight population is to avoid such products. Fresh fruit is a better option than a sweet biscuit or sticky fruit bar bearing the Tick. Salt and fatMany diet-related health problems stem from intake of salt, saturated fat and added sugar. The Heart Foundation has been strong in condemning saturated fats, and their lifestyle modifications for hypertension support choosing foods that are processed without salt. However, while the Heart Foundation quotes the number of tonnes of salt and saturated fat that have been saved by reformulating products to meet Tick criteria,3 this has little meaning when the proportion of total salt and fat consumption that these amounts represent is not provided. In any case, avoiding consumption of these reformulated products would save even more salt and saturated fat, and reduce energy intake. The Heart Foundation Tick program’s leniency for added salt is also perplexing. One mayonnaise with the Tick has more sodium than the same company’s regular brand (735 mg per 100 g v 550 mg per 100 g). Some ready-made soups with the Tick have 1280 mg sodium per serve. To put that into perspective, the adequate daily intake for sodium is 460–920 mg, and 2300 mg per day is the upper limit.4 Almost 80% of sodium that is consumed comes from processed foods. The obvious solution is to substitute processed foods with fresh foods. SugarThe Heart Foundation’s Tick criteria exclude sugar, claiming that added sugar does not differ from sugars in fruit or milk. However, fruit and milk contain a range of essential nutrients with their intrinsic sugars, whereas added sugar does not, and dietary guidelines for Australia and most other countries recommend limiting added sugar. Of 44 cereals awarded the Tick in 2011, many contain about 30% sugar. Dried fruit contributes some of this sugar, but some cereals that bear the Tick have “straight” added sugar only. At any level of energy intake, nutrient density falls as the proportion of added sugar in the diet increases.5 A recent analysis showed that intake of essential nutrients decreases significantly with each 5% increase in added sugars above 5%–10% of total energy intake,6 and the World Health Organization recommends that no more than 10% of energy should be from added sugars.7 The Tick criteria for cereals stipulate more than 50% wholegrain content. Lower levels of sugar would encourage even more of the beneficial wholegrain ingredients. Breakfast cereals with 97%–100% wholegrain content, and little or no added sugar, are popular and have no need to buy the Tick for credibility. The Heart Foundation should use these as a benchmark. ConclusionA recent editorial in the Canadian Medical Association Journal notes that partnerships between the food industry and health organisations can risk jeopardising public health goals, leading to health organisations becoming “inadvertent pitchmen for the food industry”. The authors conclude that “corporate dollars always introduce perceived or real biases that may taint or distort evidence-based lifestyle recommendations and health messages”.8 This is a particular problem when fast foods are awarded the Tick. The healthier option lures extra customers, but the bottom line is an increase in sales of regular burgers and fries. Most Australians need to eat less of almost everything except fruit and vegetables, and the new dietary guidelines for Americans have taken such recommendations on board.9 It is not a message that pleases the processed or fast food industries, but that is their problem — it is not the role of health organisations such as the Heart Foundation to keep these companies profitable. Doctors should, therefore, exercise caution when recommending products that bear the Heart Foundation Tick. The important message for Australians is that we need to change our attitude to food — from quantity to quality, and from highly processed foods to home-cooked fresh produce. The Tick is simply a distraction.

Rosemary A Stanton PhD(Hon), BSc, APD

James Tatoulis, Lyn Roberts and Anne-Marie Mackintosh argue that the Tick highlights healthier choices NO The vision of the National Heart Foundation of Australia is for Australians to have the best cardiovascular health in the world. The Heart Foundation Tick program is a cost-effective,1 population-based approach to improving the health of Australians by challenging food manufacturers and food outlets to improve the nutrition of their products.2 Doctors can be confident that the Tick signposts healthier food choices3 that have been independently tested to meet criteria for health maintenance and chronic disease prevention. The Heart Foundation recommends that products with the Tick be used in the context of a healthy eating pattern; for example, eating Tick approved fish products at least twice a week. Patients with specific dietary needs related to an illness should, as with any condition, seek tailored advice from health professionals. The Tick has proven to be popular with and trusted by Australians,4 as it provides one clear, easily identifiable symbol that highlights healthier choices without needing to read and interpret nutrition information panels and ingredient lists when shopping in supermarkets or eating out. Licensing and costsThe Tick logo is a certification trade mark, which means that the logo is registered to certify that products displaying it have met specified standards of quality and accuracy. The Heart Foundation must be able to demonstrate that these standards are met, and it is responsible for ensuring that the logo is used in accordance with the Tick criteria and regulations that govern its application. The Tick criteria are lodged with the Australian Competition and Consumer Commission. If food manufacturers fail to operate within the rules, their licence to use the Tick logo can be terminated. Manufacturers submit independent analyses, from a laboratory accredited by the National Association of Testing Authorities (NATA), to prove compliance with the Tick criteria. This process is mandatory for all food products that carry the Tick except fresh produce. Licensees sign a legal agreement to abide by the Heart Foundation’s requirements, which include compliance with Food Standards Australia New Zealand codes (Food Standards Code and Code of Practice on Nutrient Claims in Food Labels and in Advertisements), random auditing, nutrient testing, and pre-approval of labels and promotions before going to market. As the Tick is not funded by governments or by public donations, a license fee is incurred for the right to use the Tick logo. The fees are used to pay for developing nutrition criteria, laboratory analysis, and independent random auditing by SAI Global (an independent auditor), which sends auditors to “mystery shop” at food outlets. The fees for Tick approved products that are sold in supermarkets are based on a sliding scale of sales volume per annum. For food outlets, fees are based on the number of outlets and degree of auditing required. The frequency of audits is determined by SAI Global. Supermarket foods are randomly audited throughout the year, with every category audited at least once every 12 months, and all Tick approved products are analysed by the NATA-accredited company DTS Food Laboratories to ensure ongoing compliance with the applicable Tick nutrient standards. The Heart Foundation Tick program is governed by the Food Information Program Oversight Committee — a group of external honorary volunteers who report to the Heart Foundation National Board. In addition, the Criteria Working Group is responsible for developing the Tick criteria; it comprises experts in food science and technology, public health and nutrition science. No members of the Oversight Committee or Criteria Working Group have any conflicts of interest related to the food industry. Tick criteriaThe category-specific nutrient criteria5 are developed using a combination of scientific evidence, Heart Foundation position statements, key government policies, and food technology and food law considerations. The nutritional profile of foods sold in supermarkets is collected independently by Synovate Aztec (an agency that collects supermarket grocery scan data) so criteria can be set in relation to current food-purchasing trends. The criteria are made incrementally tougher. For example, the criteria for sodium levels in bread were reduced significantly for Tick approval, dropping from 450 mg per 100 g to 430 mg per 100 g in 2005, and again to 400 mg per 100 g in 2006. Tick criteria have recently been used by the federal government’s Food and Health Dialogue to help set voluntary whole-of-category targets for the food industry to meet within an agreed time frame. The Tick criteria are based on scientific evidence on chronic disease prevention,6 and include nutrients and food components deemed by the World Health Organization to be important for maintaining good health, such as fruits, vegetables, and high-fibre and wholegrain ingredients.7 They also specify sodium, saturated fat and trans fat levels, as well as energy limits and portion sizes. Although out of step with popular opinion, added sugar is not a criterion. This is because existing levels of evidence indicate that there is no direct causal relationship between added sugar and coronary heart disease,8 diabetes9 or obesity10 (with the possible exception of sugar-sweetened beverages). The sugar in Tick products may be from added sugars and/or naturally occurring sugars. The body does not differentiate their similar effects,11 and laboratory testing cannot accurately distinguish between them. Sugars — like other carbohydrates, fats, proteins and alcohol — contribute to the energy in foods; therefore, the Tick criteria limit these by setting energy limits. There is strong evidence for limiting energy intake to prevent chronic disease.12 ConclusionThe Heart Foundation Tick program has resulted in increased awareness of healthier eating and a significant reduction in saturated fats, trans fats and salt in many foods. It is also transforming the practices of food companies to benefit Australians.

James Tatoulis MS, MD, FCSANZ · Lyn M Roberts PhD · Anne-Marie Mackintosh BApplSc, PostGradDip(Diet), PostGradCert(PubRel)

Objective: To assess iodine status and the factors that influence iodine status among a cohort of pregnant women living in Gippsland.Design, participants and setting: Cross-sectional study of 86 pregnant women (at ≥ 28 weeks’ gestation) conducted in hospital antenatal care services and private obstetrician clinics across the Gippsland region of Victoria, Australia, from 13 January 2009 to 17 February 2010.Main outcome measures: Overall proportion of pregnant women with a urinary iodine concentration (UIC) > 150 μg/L; proportion of pregnant women with a UIC >150 μg/L after the mandatory iodine fortification of bread; use of supplements containing iodine; intake of foods known to be good sources of iodine; intake of bread.Results: The percentage of pregnant women with UIC >150 μg/L (indicative of iodine sufficiency) was 28%. There was no statistically significant difference in UICs before and since iodine fortification of bread. The median UIC before fortification was 96 μg/L (interquartile range [IQR], 45–153 μg/L) and since fortification was 95.5 μg/L (IQR, 60–156 μg/L). The dietary intake of iodine-rich food (including bread) and the use of appropriate supplements was insufficient to meet the increased iodine requirements during pregnancy.Conclusions: The UICs in this cohort of pregnant women are of concern, and seem unlikely to be improved by the national iodine fortification program. Pregnant women in Gippsland urgently need effective iodine education programs and encouragement to either consume iodine-rich foods or take appropriate supplements.

Ashequr Rahman MB BS, MSc, MPH · Gayle S Savige GradDipDiet, PhD · Nicholas J Deacon PhD · Janice E Chesters PhD · Barbara C Panther PhD

To the Editor: In Australia, addition of thiamine to bread flour (at 6.4 mg/kg) was made mandatory on 1 January 1991 in an effort to reduce the incidence of Wernicke’s encephalopathy and Korsakoff psychosis.1 Recently, an isocratic high-performance liquid chromatography (HPLC) method for the assessment of thiamine, thiamine monophosphate and thiamine diphosphate (TDP) in human erythrocytes has been described.2 This direct method of measuring thiamine in blood is superior to measuring red blood cell transketolase. We used an HPLC reagent kit (Chromsystems Instruments and Chemicals GmbH, Munich, Germany) to measure whole blood TDP concentrations in a population of 156 people who had alcohol use disorders. They were consecutive cases presenting between June and September 2010 at a driver assessment clinic in South Australia after they were convicted of two or more drink-driving offences. Thirty-two people taking a thiamine-containing medication or vitamin supplement were excluded. Based on the Diagnostic and statistical manual of mental disorders, fourth edition, text revision, of the remaining 124 people, 42 fulfilled criteria for “alcohol dependence” and 82 fulfilled criteria for “alcohol abuse” in the preceding 12 months.3 Of those tested, none had biochemical thiamine deficiency (defined as 2 standard deviations below the reference mean TDP concentration [< 66.5 nmol/L]). The lowest whole blood TDP concentration was 106 nmol/L. The highest concentration found was 362 nmol/L. The mean concentration was 217 nmol/L. This value is 2.5 standard deviations above the mean for the reference population (mean, 133 nmol/L; SD, 33 nmol/L).4,5 The reference range (66.5–200 nmol/L) was derived from a population that did not receive thiamine supplementation in foods. The characteristics of the distributions of thiamine concentrations in the Australian and reference populations are shown in the Box. The mean age of our population was 36 years, the youngest person was aged 19 years and the oldest, 73 years. The mean body mass index was 26.6 kg/m2 and the lowest was 18 kg/m2, so this group was not malnourished. The mean daily alcohol intake reported was 22 g/day but there was wide variation (range, 0–272 g/day; SD, 35 g/day). The results from the population with alcohol use disorders show remarkably elevated thiamine concentrations and no evidence of thiamine deficiency. The very high mean concentration of thiamine shows that this population is not at immediate risk of thiamine deficiency. It also suggests that mandatory supplementation of flour with thiamine has raised the baseline concentration of thiamine in Australians. Distribution of thiamine diphosphate (TDP) concentration in an Australian population with alcohol use disorders compared with a reference population4,5

Philip M Crowley · Matt D Gaughwin

To the Editor: Rahman and colleagues suggest that iodine deficiency in Victoria increased between 2001 and 2006, based on the findings of thyroid-stimulating hormone (TSH) levels in neonates at routine newborn screening.1 Indeed, their data as presented suggest a doubling of the percentage of mothers with iodine deficiency to over 9% during that period. This could be correct. Certainly, as they state, there is much evidence to suggest that there is mild iodine deficiency in Australia. However, there are caveats about the data they report which are not mentioned. Data from New South Wales do not show this trend. While they do suggest a degree of mild iodine deficiency, there was no increase in the percentage of neonates with TSH levels > 5 mIU/L of whole blood from 2002 to 2009 (Box), although the average age at sampling falls slightly (from 2.96 to 2.32 days) over this period. The World Health Organization has defined iodine sufficiency as being indicated, inter alia, when more than 3% of newborns aged 3–4 days have a TSH level > 5 mIU/L of whole blood.2 Factors that affect the TSH level in a newborn screening program include the precise age at sampling, and any changes to the method of TSH analysis used. In a Swiss study assessing the efficacy of iodine supplementation, there was a small but significant decrease in the TSH level from Day 3 to Day 4 of age.3 This is unsurprising: following the TSH surge in the first hours after birth, TSH levels decline gradually to a steady level at about Day 7.4 There could well have been a trend to earlier sampling in Victoria, within the bounds of the 2–4 days of age assay that Rahman and colleagues mention, over the period studied, but these crucial data are not given. The dried blood spot TSH assay method is not described either. A change in any aspect of the methodology; for example, if the manufacturer modified the antibody used, may produce a small, clinically insignificant but numerically significant, change in results. If the data presented by Rahman and colleagues for Victoria do not have these biases, then the situation warrants further investigation, but whatever is happening in Victoria seems not to be replicated over the border. Percentage of newborns with thyroid-stimulating hormone (TSH) level > 5 mIU/L of whole blood, detected by routine newborn screening in New South Wales, by year Year Newborns with TSH level > 5 mIU/L 2002 3.80% 2003 3.68% 2004 3.87% 2005 5.02% 2006 4.48% 2007 3.56% 2008 3.92% 2009 4.00%

Bridget M Wilcken · Veronica C Wiley

In reply: The methods used for blood sample collection and analysis remained unchanged during our data collection period. One source of thyroid-stimulating hormone (TSH) calibrators and reagents was used over the study period by a single laboratory covering all of Victoria. Material from the United States Centers for Disease Control and Prevention was used for external quality assurance, ensuring that the results were in agreement with those of other laboratories. The per cent coefficient of variation over the period ranged from 10% to 20%. The table of neonatal TSH values for New South Wales provided by Wilcken and Wiley further demonstrates the value of using TSH levels as a screening tool for population iodine status, even with a decreasing mean age of sample collection. While we dealt with the effect of sample collection time in our published article,1 here we present a table illustrating analysis of the Victorian neonatal TSH values for samples collected at 48, 72 and 96 hours after birth (Box). The percentage of elevated TSH values increased from 2001 to 2006 at each collection time and, although the percentage of elevated TSH values decreased with increasing age, these values were still indicative of iodine deficiency. Iodine status varies between regions. The National Iodine Nutrition Study (NINS) found both South Australia and Queensland iodine sufficient, while the neighbouring states of NSW and Victoria were iodine deficient.2 The results also indicated that iodine status was worse in Victoria than in NSW; therefore, we might expect similar differences in TSH values. We are now in the process of analysing Victorian TSH values for 2007 to 2010. Percentage of newborns with thyroid-stimulating hormone (TSH) level > 5 mIU/L for blood samples collected at 48, 72 and 96 hours after birth, Victoria, 2001–2006 Sample collection time (h) Percentage of neonates with TSH > 5 mIU/L according to birth year 2001 2002 2003 2004 2005 2006 48 5.73% 6.83% 8.47% 10.58% 11.86% 13.53% 72 4.20% 5.15% 6.87% 7.01% 9.13% 9.38% 96 2.49% 3.21% 4.37% 3.78% 5.98% 5.34%

Ashequr Rahman · Gayle S Savige · Nicholas J Deacon · Ivan Francis · Janice E Chesters

Objective: To determine the iodine status of participants in the Aboriginal Birth Cohort Study who resided in the Darwin Health Region (DHR) in the “Top End” of the Northern Territory prior to the introduction of mandatory iodine fortification of bread.Design, setting and participants: Participants in our study had been recruited at birth and were followed up at a mean age of 17.8 years. Spot urine samples were collected and assessed for iodine concentration at a reference laboratory. The median urinary iodine concentration (MUIC) of residents of the DHR was calculated and compared with international criteria for iodine status. Analyses were conducted for subgroups living in urban areas (Darwin–Palmerston) and remote communities (rural with an Aboriginal council). We collected a repeat sample in a subset of participants to explore the impact of within-person variation on the results.Main outcome measure: MUIC for residents of the DHR.Results: Urine specimens were provided by 376 participants in the DHR. Overall MUIC was 58 μg/L when weighted to the 2006 Census population. Urban boys had higher values (MUIC = 77 μg/L) than urban and remote-dwelling non-pregnant girls (MUIC = 55 μg/L), but all these groups were classified as mildly iodine deficient. Remote-dwelling boys had the lowest MUIC (47 μg/L, moderate deficiency). Pregnant girls and those with infants aged less than 6 months also had insufficient iodine status. Correction for within-person variation reduced the spread of the population distribution.Conclusions: Previously, iodine deficiency was thought to occur only in the south-eastern states of Australia. This is the first report of iodine deficiency occurring in residents of the NT. It is also the first study of iodine status in a defined Indigenous population. Future follow-up will reassess iodine status in this group after the introduction of iodine fortification of bread.

Dorothy E M Mackerras MPH, PhD · Gurmeet R Singh MPH · Creswell J Eastman MD, FRACP, FRCPA

Objective: To determine the impact that mandatory fortification with folic acid of wheat flour used in breadmaking has had on the blood folate levels of an Australian population since it was introduced in September 2009.Design, setting and patients: A retrospective analysis of serum and red blood cell (RBC) folate levels of 20 592 blood samples collected between April 2007 and April 2010 from a wide variety of inpatients and outpatients and analysed in a large public hospital diagnostic pathology laboratory.Main outcome measures: Prevalences of low levels of serum and RBC folate and monthly mean levels before and after introduction of mandatory fortification.Results: Between April 2009 and April 2010, there was a 77% reduction in the prevalence of low serum folate levels (from 9.3% to 2.1%) in all samples tested and an 85% reduction in the prevalence of low RBC folate levels (from 3.4% to 0.5%). In April 2010, the prevalence of low RBC folate levels for females of childbearing age was 0.16% for all samples. There was a 31% increase in mean serum folate level (from 17.7 nmol/L to 23.1 nmol/L; t = 9.3, P < 0.01), and a 22% increase in mean RBC folate level (from 881 nmol/L to 1071 nmol/L). The greatest increment in mean serum folate levels occurred in September 2009, the month that mandatory fortification was introduced, although there was evidence of a gradual change during the preceding months.Conclusion: The introduction of mandatory fortification with folic acid has significantly reduced the prevalence of folate deficiency in Australia, including in women of childbearing age.

Ross D Brown PhD, MBA, FAIMS · Mark R Langshaw BAppSci, GradDipIT · Elaine J Uhr MSc(BiolSc) · John N Gibson PhD, FRACP, FRCPA · Douglas E Joshua DPhil, FRACP, FRCPA

Obesity, linked to chronic disease, and global warming, linked to climate change, may be indicators of serious problems with our consumption-based economic system About 15% of the world’s population are now overweight or obese, and this is considered to be a factor in the rising incidence of chronic diseases.1 Excessive carbon concentrations now also exist in the atmosphere (50% higher now than 50 years ago), with implications for the environment and climate disruption.2 Although it is not immediately obvious, there is a connection between these two phenomena, with energy being the common factor — excess energy intake over expenditure in the case of obesity, and excess carbon from energy sources over the capacity of environmental “sinks” (oceans, soil, plants) to absorb carbon in the case of the environment. This suggests there may be a common distal driver, in which case obesity and global warming could be symptoms of a broader environmental disorder — similar “canaries” in the same “mineshaft”. Body fat in humans is essential for survival. Too little causes health problems (insulin resistance, type 2 diabetes, etc), as does too much. Unknown factors (probably genetic) seem to define a point — which may vary widely between individuals — beyond which further expansion of fat cells is limited, leading to a “spillover” of excess fat into ectopic stores (muscle, blood, viscera, etc). Before this point is reached, fat stores seem to be benign, or even healthy,3 even in some obese individuals. Beyond this, fat appears to become toxic, and to become linked to chronic disease,4 possibly through the medium of a form of low-grade systemic inflammation, or “metaflammation”.5 Metaflammation was shown over a decade ago to be distinct from classical inflammation. It seems to be caused not just by “spillover” fat, but also by lifestyle and environmental factors, some of which can cause obesity (poor diet, inactivity, inadequate sleep, etc), but many of which may not.6 Non-alcoholic fatty liver disease (NAFLD), often a precursor to chronic disease in the presence of such lifestyle behaviours without obesity7 or visceral fat,8 supports this idea, as does a reduction in NAFLD with exercise independent of weight loss.9 In this sense, obesity might be just a canary in a mineshaft, signalling bigger problems in the overall environment. But if obesity is the canary, what constitutes the mineshaft? A clue can be gained from looking at pro- and anti-metaflammatory stimuli. We have suggested elsewhere10 that pro-inflammatory “inducers”11 are new, arising as a result of the industrial revolution of the late 19th century, whereas those that are anti-inflammatory (or neutral versions of those causing inflammation) have been familiar to humans for thousands of years. The hypothesis proposed from this is that the human immune system reacts (albeit at a lower level than to injury or microbial invasion) to stimuli to which it has not had time to adapt.12 Metaflammation is thus to chronic disease what inflammation is to injury and acute disease. Inflammation normally relates to a physiological condition. However, it can apply, at least metaphorically, to the external (ecological), as well as the internal (biological) environment. The body is unable to “soak up” glucose as a result of insulin resistance, and this leads to metaflammation and biological abnormalities in the form of chronic diseases. In the broader ecological environment, the biosphere is unable to soak up or “sequester” carbon dioxide (and other greenhouse gases) because environmental sinks are overwhelmed by emissions from the oxidation of fossil fuels,2 resulting in a form of inflammation and “carbon resistance” in the ecosphere. This leads to potential ecological “abnormalities” that are metaphorically similar to the chronic diseases related to insulin resistance. Our metaphorical mineshaft can be identified by tracking back the causes of both forms of “inflammation” in a classical epidemiological fashion, as shown in the Box. From this, it is clear that the mineshaft is the modern postindustrial environment, in which a principal driver has been the system of exponential economic growth, particularly that driven by the use of fossil fuels. But how can something that has been so good for human health and wellbeing as economic growth be regarded as negative? The answer lies in the inherent dynamism of any growth system. There is little doubt that growth has been the biggest single contributor to human health in history.13 However, any form of exponential growth must eventually meet its limits. Leading up to this, one might expect to see diminishing returns on investment. In terms of health, this time may have arrived. Data from Sweden, the United Kingdom and other countries over the past 200 years show an initial close relationship between health and growth, but since the 1970s, a reversed relationship, in which further growth results in reduced progress in health.14 Increases in obesity, which follow from the consumption required to feed the growth system beyond the “epidemiological transition” (where the incidence of chronic diseases surpasses that of infectious diseases)15 in developing countries, is one consequence. Greenhouse gas emissions, which are related to the consumption driving obesity, also closely follow the business cycle at the micro level, as well as the growth in gross domestic product (GDP) at the macro level.16 A “sweet spot”17 in the material phase of growth therefore appears to have been reached and, in some aspects, overshot in developed countries, as reflected by the diminishing rate of return in health, as well as ecological wellbeing, from further growth. Obesity (and greenhouse gases), within this framework, represents a canary. In times past, canaries were taken into mineshafts to warn of problems with air quality, indicated by their sudden collapse. The mineshaft in our metaphor is the economic system — specifically monetary growth, as measured in terms of GDP and its consequent consumption — that drives the modern industrial environment. To attribute the epidemic in chronic disease to this is not fanciful. It is clear from the lessons of developing countries like India and China that chronic diseases are related to changes that occur with economic development past a certain point — the epidemiological transition. The fact that chronic diseases begin to increase rapidly around the same time as a society’s carbon footprint begins to grow is not coincidental. Unsequestered greenhouse gas emissions are the manifestation of a mineshaft of growth beyond a threshold of positive returns. Obesity — and climate change — are merely “collateral damage in the struggle for modernity”.17 The dramatic worldwide increase in obesity is the most visible biological warning that our consumer-driven, macroeconomic environment (the mineshaft) is in need of an overhaul. While it is imperative for us to keep trying, attempts to reduce obesity at the population level, and to control climate change at the world level, without dealing with these broader economic and environmental issues, is like trying to resuscitate an asphyxiated canary while leaving untouched the mineshaft that caused the asphyxiation. Epidemiological course of biological and ecological “inflammatory” processes

Garry J Egger MPH, PhD · John B Dixon MB BS, PhD, FRACGP

Objective: To use neonatal thyroid-stimulating hormone (TSH) concentration data to measure the iodine status of the population of the Australian state of Victoria.Design, participants and setting: Retrospective analysis of the results of 368 552 neonatal heel-prick blood tests for TSH concentration in Victoria in the years 2001–2006.Main outcome measures: Iodine deficiency as indicated by a mean percentage of neonatal TSH concentrations > 5 mIU/L of over 3% in accordance with World Health Organization, United Nations Children’s Fund and International Council for the Control of Iodine Deficiency Disorder criteria; comparison of findings for the nine Department of Human Services health regions in Victoria.Results: The mean percentage of neonatal TSH concentrations > 5 mIU/L ranged from 4.07% in 2001 to 9.65% in 2006, and this increase was statistically significant (P < 0.001). The populations of all nine Victorian health regions showed increasing iodine deficiency over the study period. Metropolitan populations had higher iodine deficiency than non-metropolitan populations, and this difference was also statistically significant (P < 0.05). These results are consistent with urinary iodine excretion research in Victoria.Conclusions: The high percentage of elevated TSH concentrations among newborns is of concern and requires ongoing monitoring. Neonatal TSH assay is part of routine screening in Australia, and thus offers an effective and economical method of monitoring population iodine status.

Ashequr Rahman MB BS, MSc, MPH · Gayle S Savige PhD · Nicholas J Deacon PhD · Ivan Francis BSc, GradDipCompSci · Janice E Chesters PhD

To the Editor: We report a case of ischaemic stroke in a 34-year-old man with severe vitamin C deficiency caused by poor nutrition. The patient was a lifelong non-smoker with no history of hypertension or hypercholesterolaemia, and no family history of stroke, although he had recently been diagnosed with type 2 diabetes mellitus. At presentation, neurological examination showed profound left-sided hemiparesis, with normal sensory examination and visual fields. Cardiovascular examination was normal, and there were no carotid bruits. The patient’s body mass index was 25.5 kg/m2. Magnetic resonance imaging of of his brain showed acute infarction in the right posterior corona radiata (Box, A). Coagulation and lipid profiles were normal. Glycosylated haemoglobin was 7.1%. Comprehensive testing for underlying thrombophilia, vasculitides and Fabry disease all returned negative results. Computed tomography angiography and carotid ultrasonography confirmed normal carotid and vertebral arteries. Transoesophageal echocardiography showed a structurally normal heart without a source of embolus. The patient had poor dentition, with calculus deposition, scorbutic gums and gingival inflammation (Box, B), and reported easy bruising in recent months. Suspecting a diagnosis of scurvy, we conducted a nutritional assessment of the patient. His diet consisted mainly of fast food, with negligible vegetable and fruit intake, and no vitamin supplementation. For the week before admission, we determined that his average vitamin C intake was 4 mg/day. This corresponded to a > 99% probability of inadequate intake when compared with the estimated average requirement of 30 mg/day for adults1 (z = − 4.33; P = 0.0015). Laboratory testing confirmed the presence of severe vitamin C deficiency (< 5 μmol/L; reference range, 40–100 µmol/L). The patient was admitted to a stroke unit, commenced on aspirin, ramipril and atorvastatin, and received dietary counselling. Vitamin C 1000 mg daily was prescribed for one month. Subsequent testing confirmed normalisation of his plasma vitamin C. Following inpatient rehabilitation, he regained motor function and returned to independent living. There is growing evidence that vitamin C deficiency is an important, but largely unrecognised, risk factor for modification in patients with cerebrovascular disease.2 Vitamin C is a water-soluble antioxidant that inhibits oxidation of low-density lipoprotein and protects against endothelial dysfunction. Primate models have confirmed that cerebral infarct size is inversely related to cerebral vitamin C content.3 Although scurvy is now relatively rare, subclinical vitamin C deficiency is not uncommon, being present in about 10% of the general population.4 Alcoholics, institutionalised and elderly people are particularly at risk. In this case, we hypothesise that an unhealthy diet resulted in deficiencies in antioxidants (including vitamin C), and that this contributed to stroke pathogenesis. The marked prematurity of disease onset may have resulted from effect modification of antioxidant deficiency on conventional atherosclerotic risk factors (such as diabetes). A cohort study previously observed the modifying effect of vitamin C deficiency on the association between stroke and hypertension.5 However, it is unlikely that a direct causal link will ever be established. Since malnutrition and unhealthy eating practices continue to be serious public health problems, we suggest attention to nutritional status should be incorporated into the new standard of stroke care. Perhaps a new adage should be considered: an orange a day keeps stroke away? A: Diffusion-weighted magnetic resonance image of the patient’s brain showing an acute infarction in the posterior limb of the right corona radiata. B: The patient’s mouth showing scorbutic gums consistent with scurvy.

Emily Y-J He · Louis W Wang · Matthew C Kiernan