Endocrinology

To the Editor: In describing 8 years of experience in managing adolescent gender identity disorder (GID) at a paediatric hospital clinic, Hewitt and colleagues highlight a small group of patients who require momentous life-long clinical decisions made in a timely manner.1 However, the rarity of this condition means that experience in any centre is limited. The authors state that authorisation from the Family Court of Australia is ...

Ann J Conway · Julie C Hamblin · David J Handelsman

To the Editor: I welcome the article by Hewitt and colleagues,1 but their protocol is problematic. Suppression of puberty improves mental health and general functioning, but not body image and dysphoria.2 For this, cross-sex hormones and/or surgery are the only effective treatments.2 Withholding cross-sex hormones until children are 16 years of age may worsen their mental health,3 cause resentment, and encourage self-medication. Increasingly, young transsexual people are ...

Zoë Hyde

In reply: We thank Hyde and Conway and colleagues for their correspondence following our report on treatment for young people with gender identity disorder (GID).1 We follow current international consensus recommendations for management,2,3 but accept that as more research is performed, there may be future adjustments to endorsed protocols. At present, patients can apply to the Family Court of Australia for authorisation of treatment that ...

Jacqueline K Hewitt · Campbell Paul · Louise K Newman

Are current standards of evidence always appropriate when making the decision to subsidise treatment?

Wendy L Lipworth MB BS, MSc, PhD · Ken Ho MD, FRACP, FRCP · Ian H Kerridge BMed(Hons), MPhil, FRACP · Richard O Day AM, MD, FRACP

Appropriate assessment and management of diabetes-related foot ulcers (DRFUs) is essential to reduce amputation risk. Management requires debridement, wound dressing, pressure off-loading, good glycaemic control and potentially antibiotic therapy and vascular intervention. As a minimum, all DRFUs should be managed by a doctor and a podiatrist and/or wound care nurse. Health professionals unable to provide appropriate care for people with DRFUs should ...

Shan M Bergin BAppSci(Pod), PhD · Joel M Gurr BSc(Pod), MBA · Bernard P Allard MB BS, FRACS(Vasc) · Emma L Holland RN, CDE, MA(Ed) · Mark W Horsley MB BS, FRACS(Ortho) · Maarten C Kamp FRACP, MHA, GAICD · Peter A Lazzarini BAppSci(Pod) · Vanessa L Nube DipAppSci(Pod), MSc(Med) · Ashim K Sinha MB BS, MD, FRACP · Jason T Warnock DipAppSc(Chir), GradCertDiabEd · Jan B Alford RN, MEd(AdEd), CDE · Paul R Wraight MB BS, FRACP, PhD

Objective: To identify a level of iodine supplementation to recommend for pregnant and breastfeeding women in Australia.Design, setting and participants: Dietary modelling indicated that mandatory fortification of bread with iodine by replacing salt with iodised salt would still leave a gap in iodine intakes in pregnant and breastfeeding women in Australia. Iodine shortfall was estimated by two separate methods: (i) analysis ...

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

The burden of type 2 diabetes mellitus (T2DM) among Indigenous children and adolescents is much greater than in non-Indigenous young people and appears to be rising, although data on epidemiology and complications are limited. Young Indigenous people living in remote areas appear to be at excess risk of T2DM. Most young Indigenous people with T2DM are asymptomatic at diagnosis and typically have a family history ...

Peter Azzopardi MB BS, MEpi, FRACP · Alex D Brown BMed, MPH, PhD · Paul Zimmet MD, PhD, FRACP · Rose E Fahy MB BCh, FRACP, MRCP · Glynis A Dent Grad Cert Diabetes Education, Grad Cert Human Nutrition · Martin J Kelly MB BS, FACRRM, PhD · Kira Kranzusch MB BS, FRACP · Louise J Maple-Brown MB BS, FRACP, PhD · Victor Nossar MB BS, FRACP, FAFPHM · Martin Silink MD, FRACP · Ashim K Sinha MB BS, MD, FRACP · Monique L Stone MB BS, FRACP, MD · Sarah J Wren MHSc (Nursing), Grad Cert Diabetes Education

To the Editor: A 24-year-old Sudanese woman presented to her general practitioner in 2011 with one month of fatigue, dizziness, abdominal distension and facial oedema. Hypocortisolaemia was present: morning cortisol, 13 nmol/L (reference interval [RI], 240–620 nmol/L), afternoon cortisol, 9 nmol/L (RI, 100–280 nmol/L). In contrast to this profile, she appeared cushingoid (moon facies, central obesity, skin fragility and striae) with skin depigmentation on her face, back and hands (Box, A). ...

Rebecca F Goldstein · Helena J Teede · Carolyn A Allan

Objective: To describe patterns of testosterone prescribing in Australia over the past two decades by state or territory and by product type.Design and setting: Observational analysis of testosterone prescribing data obtained from two independent data sources — the Pharmaceutical Benefits Scheme (PBS) and IMS, a source of commercial pharmaceutical sales data.Main ...

David J Handelsman MB BS, FRACP, PhD

To the Editor: We read Scott and Harris’s1 article with great interest and agree that new funding models for diabetes care must be carefully designed to ensure that interventions are effective. For this reason, the Diabetes Care Project2 (formerly the Coordinated Care for Diabetes Pilot) developed pilot interventions following reviews of international trials and extensive ...

Tim Fountaine · Jonathan E Shaw · Paul Z Zimmet

Objective: To determine the incidence of and factors associated with vitamin D deficiency rickets in Australian children.Design: 18-month questionnaire-based prospective observational study, using Australian Paediatric Surveillance Unit (APSU) data.Setting: ...

on behalf of the APSU Vitamin D Study Group

Objective: To determine if the improvement in inpatient glycaemic control observed with basal–bolus insulin (BBI) over sliding-scale insulin (SSI) in the formal study setting translates to routine clinical conditions.Design, setting and patients: Cross-sectional study in which capillary blood glucose levels (BGLs) were prospectively measured four times daily for up to 8 days in 124 patients with type 2 diabetes admitted to a tertiary teaching hospital and treated with BBI between November 2008 and May 2010. Data from the BBI treatment group were compared with retrospective data from 96 patients treated with SSI between June 2001 and May 2006.Main outcome measures: Mean daily BGL; independent effect of insulin regimen on mean daily BGL.Results: Mean baseline BGL was not significantly different in patients receiving BBI and SSI (mean ± SD, 11.3 ± 4.1 v 10.6 ± 4.3 mmol/L; P = 0.23). After the first full day of therapy, mean daily BGL for patients receiving BBI was 1.6 ± 3.7 mmol/L lower than baseline BGL, and it remained 1.6–2.4 mmol/L lower than baseline throughout the study (P < 0.001). In contrast, there was no significant change in BGL for patients receiving SSI. Random effects regression analysis indicated that BBI was associated with a significantly lower mean daily BGL than SSI, independent of other variables (P < 0.001). The incidence of hypoglycaemia (BGL < 4 mmol/L) was significantly greater in patients receiving BBI than SSI (3.3% v 1.4%; P < 0.001), but there was no significant difference for severe hypoglycaemia (BGL < 2.8 mmol/L) (0.3 v 0.5%; P = 0.3).Conclusions: Under routine clinical conditions, BBI is effective and safe across a range of patients and appears to be superior to SSI. Clinical improvements reflected those seen in a strict formal study setting.

Greg W Roberts BPharm, FSHP · Norma Aguilar-Loza BN(Hon) · Adrian Esterman PhD · Morton G Burt MB ChB, PhD · Stephen N Stranks MB BS

Non-surgical intervention has many benefits. A recent article published in the Journal1 was widely reported in the popular press, with statements such as the following being quoted: public health messages encouraging people to eat healthy food and to exercise are unlikely to have long-term impact on their weight....

Daniel J Green PhD · Andrew J Maiorana PhD

To the Editor: We recently reviewed the individual policies of seven Australian tertiary maternity hospitals, from across all states, regarding neonatal vitamin D supplementation. An Australian 2006 consensus statement concerning the treatment and prevention of vitamin D deficiency in children and neonates identified the need to implement vitamin D supplementation in neonates born to mothers with serum 25-hydroxyvitamin D (25-OHD) levels of ≤ 50 nmol/L.1 Despite this, we found that a number of institutions have recently adopted a policy of treating infants of mothers with an antenatal serum 25-OHD level of < 75 nmol/L. Treatment of the neonate is with oral stoss therapy (50 000 IU vitamin D as a single dose) and/or daily oral vitamin D therapy (1000 IU) until cessation of breastfeeding. It should be noted that previous research has suggested that a substantial proportion of Australian women of childbearing age have a serum 25-OHD level < 75 nmol/L.2 Vitamin D is a pleiotropic hormone that influences the expression of more than 200 human genes.3 It has a wide range of biological actions, and the full implications of vitamin D supplementation during early life are unknown. While it is clear that very low levels of vitamin D are associated with abnormal bone development and the risk of hypocalcaemic seizures, it is also possible that vitamin D supplementation may have adverse effects. For example, we and others have found that a history of vitamin D supplementation during early life may be associated with an increase in allergic outcomes such as asthma and hayfever in later life.4,5 These are observational findings, limited by potential confounding and reverse causation, but they highlight the potential concern of changes in medical practice without an accompanying updated evidence base. There is an urgent need for improved data and further debate before implementing a public health policy affecting as many as half of all Australian infants. In the interim, we would advocate treatment of neonates only if they fall within the 2006 guidelines (mother’s serum 25-OHD ≤ 50 nmol/L).

Kate M McCloskey · Natalie Wright · Anne-Louise Ponsonby · Peter J Vuillermin

Should the recently published PCOS guidelines be revised? The recent supplement of the Journal titled “Assessment and management of polycystic ovary syndrome: summary of an evidence-based guideline” summarises the full Australian guideline document that was launched at the 2011 Endocrine Society of Australia Annual Scientific Meeting.1 The document is thorough and has been put together meticulously; it covers the major diagnostic and management issues encountered by health professionals looking after patients with this challenging condition. However, the recommendations for metabolic screening included a 2-yearly 75 g oral glucose tolerance test (OGTT) in all women with polycystic ovary syndrome (PCOS), and annual testing for those with an additional risk factor.1 I believe that this screening protocol is not based on evidence and should not be applied universally to women with PCOS. Insulin resistance is a common feature in PCOS, and many studies have shown that even lean women with PCOS are insulin resistant compared with weight-matched controls.2 However, although the major risk factors for abnormalities in glucose metabolism are amplified in these women, they are similar to those in the general population — namely age, obesity and family history of type 2 diabetes.3 Given the young age of many patients with PCOS, and the fact that a significant minority (34% in one United States study4) have a normal body mass index (BMI), the diagnostic yield of 2-yearly OGTTs in some subgroups of women with PCOS is very low. The recommendation was taken directly from a position statement that was published by the Androgen Excess Society in 2007, in which it was acknowledged that some members of the expert panel disagreed with the recommendation and suggested a more targeted approach to screening.5 In a study of 372 Australian women with PCOS, only one of 73 women who had been diagnosed with diabetes had a BMI of less than 25 kg/m2, but, in women in the cohort who were aged under 30 years (whose mean BMI was over 35 kg/m2), the prevalence of diabetes was less than 2%.3 Therefore 98% of women with PCOS under the age of 30 years could undergo an OGTT five times during their 20s with little chance of a clinical benefit. Should screening for impaired glucose tolerance, which is more common, be a sufficient reason to justify routine screening? In the same Australian study, the prevalence of impaired glucose tolerance in a very obese group was 13.4%.3 A more recent report from the US showed that only 3% of non-diabetic women with PCOS and a BMI of less than 25 kg/m2 had impaired glucose tolerance.6 Furthermore, among the principles of screening are (i) that there must be evidence that diagnosing the condition being screened for leads to treatment which is better at an earlier stage and (ii) that there should be an agreed policy on who to treat.7 Such evidence does not exist for impaired glucose tolerance screening in PCOS. Possible predictors of progression from normal glucose tolerance to abnormal glucose metabolism in PCOS have been examined. In a Canadian cohort of patients with PCOS, the best predictor of later abnormal glucose tolerance was a glucose excursion of more than 1.4 mmol/L in the initial OGTT (ie, that which returned a normal result).8 Confining future screening to those women who fulfilled this criterion would reduce the number of the OGTTs performed by 45%.8 Decision tree modelling is another technique that has been used to enable targeted screening of women with PCOS.9 Even a decision tree which uses clinical data alone (ie, age, BMI, waist circumference and waist-to-hip ratio) would reduce the number of OGTTs performed by 25%, without missing a single case of impaired glucose metabolism.9 While intuitively it would seem that delaying or preventing the diagnosis of diabetes would be good, in practice this just means a change in the glucose threshold at which intervention commences. Considering that recent large studies of type 2 diabetes have shown no evidence that aggressive glucose lowering improves macrovascular outcomes, and that it may increase mortality,10,11 we are far from a situation where earlier glucose lowering intervention in “prediabetes” is of proven benefit. The mainstay of treating patients with impaired glucose tolerance is lifestyle change and, in some cases, metformin therapy12 — established therapies for PCOS that are covered later in the guideline document.1 Some experts have stated that metformin should only be used to treat PCOS in the settings of diabetes and impaired glucose tolerance (and possibly in adolescence) and should not be used to manage infertility or hirsutism.13 This is a narrower opinion than expressed in the Australian guideline and ignores the beneficial effects that metformin may have in inducing ovulation in women with a BMI of less than 30 kg/m2 or when combined with clomiphene citrate.1 Diagnosing impaired glucose tolerance in PCOS may not lead to any particular change in management, with lifestyle change and/or metformin still the mainstay. The exception to this is women seeking to become pregnant, in whom early recognition of an abnormality in glucose metabolism enables earlier treatment and improved fetal and maternal outcomes. Predominantly though, the main diagnosis of importance from an intervention viewpoint is type 2 diabetes. My concern is that practitioners who choose to perform selective OGTT screening in patients with PCOS (based on age, BMI, waist circumference, family history of diabetes and a wish to become pregnant) will be seen as “not following the guidelines”. Patients do not find the OGTT a pleasant experience. Non-selective, frequent repetition of the OGTT in women with PCOS will create an unnecessary burden for many patients, with no proven benefit. Larger prospective studies are needed to examine whether the intensive screening protocols recommended in the Australian guideline and the intervention which arises from an abnormal result are superior to universal lifestyle advice and selective screening of women with PCOS who have a substantially increased risk of diabetes. I urge the authors of this otherwise excellent document to revise their recommendations to state that performing a 2-yearly OGTT in all women with PCOS has an extremely low yield of abnormality in certain subgroups and that no evidence of benefit exists in diagnosing impaired glucose tolerance over and above the usual treatment recommended for this common condition. Until such evidence is available, a more targeted approach to screening for glucose metabolism abnormalities in PCOS should be suggested.

Warrick J Inder MB ChB, MD, FRACP

Incorrect symbol: In the supplement to the 19 September 2011 issue of the Journal, “Assessment and management of polycystic ovary syndrome: summary of an evidence-based guideline” (Med J Aust 2011; 195: S65-S112), there was an error in Algorithm 5. Under Pharmacological management, the third evidence-based recommendation contained a ≥ symbol instead of a ≤ symbol. The recommendation should read: Metformin could be used alone to improve ovulation rate and pregnancy rate in women with PCOS who are anovulatory, have a BMI ≤ 30 kg/m2 and are infertile with no other infertility factors. The html and pdf versions of this article have been corrected.

Helena J Teede · Marie L Misso · Amanda A Deeks · Lisa J Moran · Bronwyn G A Stuckey · Jennifer L A Wong · Robert J Norman · Michael F Costello

To the Editor: I would like to add some detail to the article by Shaw and colleagues1 on the costs of screening for diabetes and glycated haemoglobin (HbA1c) testing. At face value, using the 85% Medicare Benefits Schedule (MBS) rebate, the item for HbA1c testing costs $1.85 less than the item for a glucose tolerance test (more than 10% cheaper), but it is a little more complicated than these simple figures suggest. In 2010, 295 023 glucose tolerance tests (item number 66542) were claimed on the MBS — up 61% on the number ordered in 2004 (183 090)2 — which reflects the increase in ordering by general practitioners, who I believe are more aware of the increased incidence and prevalence of one of the most common chronic diseases in Australia. I also believe that it reflects the use of the glucose tolerance test as the definitive test for diabetes (rather than relying on a single fasting glucose level) in private practice. In contrast, 1 021 247 HbA1c tests (item number 66551) were claimed in 2010, versus 911 623 in 2004 — up by only 12% over the same 7-year period.2 This reflects “coning” of pathology items in the MBS. There are two types of cone that affect billing of HbA1c tests: the “grand cone”, which restricts billing to the three most expensive items ordered by a GP on a single occasion (regardless of the number of tests ordered), and the “temporal cone”, where only four HbA1c tests can be billed in any 1 year. The glucose tolerance test has no temporal restrictions and is usually performed on its own, so it avoids the grand cone, but the HbA1c test is often ordered with a bank of other tests (eg, as part of diabetes monitoring) and is thus not usually billed to Medicare. In my practice, only 30% of reported HbA1c tests can be billed to Medicare, hence the cost to Medicare per reportable test is about a third of the listed rebate of $14.40. Furthermore, as Shaw et al point out, HbA1c testing cannot currently be billed for the diagnosis of diabetes, although my personal observation is that many doctors are already using this as a screening test. There are essentially three powerful drivers for HbA1c testing: the increased prevalence of diabetes, the (honest) push to test HbA1c levels every 4 months (through care plans etc) and the use of HbA1c tests to diagnose diabetes. I believe that Medicare currently pays for less than 40% of these tests and that this proportion will fall as more HbA1c tests are requested. The majority of the costs for HbA1c testing are subsidised by pathology practices — which, philosophically, I find quite odd. These points need to be taken into account when undertaking a cost–benefit analysis of screening for diabetes in Australia.

Len D Moaven

To the Editor: The position statement by Jones and colleagues regarding the change of HbA1c reporting to the new Système International (SI) units — which has been recommended by the Australasian Association of Clinical Biochemists, the Australian Diabetes Educators Association, the Australian Diabetes Society and the Royal College of Pathologists of Australasia — provides a comprehensive summary of the rationale behind the proposed change and suggests a 2-year period of dual reporting.1 However, Jones et al did not specify targets for children and adolescents, and we believe that it is important to do so. The incidence of type 1 diabetes in Australian children and adolescents is among the highest in the world2 and, in New South Wales, type 2 diabetes represents at least 10% of cases of new-onset diabetes in adolescents.3 National evidence-based clinical care guidelines for type 1 diabetes in children, adolescents and adults4 include age-specific targets for HbA1c, while recognising that such targets are predominantly consensus based. HbA1c targets for young people with type 1 diabetes are higher, with a level of < 7.5% recommended for children and adolescents in the Australian guidelines4 and in those produced by the International Society for Pediatric and Adolescent Diabetes (ISPAD).5 Jones et al note that “Achievement of HbA1c targets must be balanced against risk of severe hypoglycaemia, especially among older people”;1 this is also the case for young people. For children and adolescents with type 2 diabetes, the ISPAD guidelines recommend an HbA1c target of < 7%.5 The move to SI units represents a major change in the established, widely recognised outcome measure of glycaemia; during the transition period, the specific needs of young people with diabetes must not be forgotten.

Maria E Craig · Kim C Donaghue · Fergus J Cameron · Martin Silink

In reply: We appreciate Craig and colleagues’ comments regarding the importance of reporting general HbA1c targets for children and adolescents with type 1 and type 2 diabetes. In our position statement, the headings of Box 2 and Box 3 indicated that the targets listed were for adults with type 1 diabetes and adults with type 2 diabetes, respectively.1 While it is not possible to highlight every clinical situation, we agree that providing general HbA1c targets for children and adolescents will add value to our article, and we have updated it accordingly,1 recognising the differences in these targets for type 1 diabetes (≤ 58 mmol/mol, ≤ 7.5%) and type 2 diabetes (≤ 53 mmol/mol, ≤ 7.0%).2-4 In the interests of uniformity and simplicity, the paediatric targets expressed as “<”2-4 have been adjusted to “≤”, which represents differences of less than 1.5% of the target values. Addendum p 524

Graham R D Jones · George Barker · Ian Goodall · Hans-Gerhard Schneider · Mark D S Shephard · Stephen M Twigg

AddendumHbA1c targets for young people not specified: In the position statement “Change of HbA1c reporting to the new SI units” in the 4 July 2011 issue of the Journal (Med J Aust 2011; 195: 45-46), HbA1c targets for young people with diabetes were not specified. The following HbA1c target ranges have been added to Boxes 2 and 3, respectively: for children and adolescents with type 1 diabetes, ≤ 58 mmol/mol (≤ 7.5%); for children and adolescents with type 2 diabetes, ≤ 53 mmol/mol (≤ 7.0%). Further details are published in this issue of the Journal.

Graham R D Jones · George Barker · Ian Goodall · Hans-Gerhard Schneider · Mark D S Shephard · Stephen M Twigg

To the Editor: We wish to report Queensland data regarding vitamin D levels during pregnancy, to contribute to the debate on screening during pregnancy raised in Lau and colleagues’ article1 and Ebeling’s accompanying editorial.2 In 2009, we measured serum 25-hydroxyvitamin D (25[OH]D) levels, using a DiaSorin radioimmunoassay (DiaSorin, Stillwater, Minn, USA), in 75 women who attended general antenatal clinics at the Royal Brisbane and Women’s Hospital (RBWH) and Mater Mothers’ Hospital. Both institutions’ Human Research Ethics Committees approved the study. Participants gave written consent. The RBWH Private Practice Fund covered pathology expenses. Fifty-seven of the 75 women were white; the remainder were Asian (five), Indian Subcontinental (seven), Polynesian (four), Middle Eastern (one) and black African (one). Mean age was 28.6 years (SD, 5.4 years), mean gestational age was 28.7 weeks (SD, 2.7 weeks) and mean body mass index was 26.4 kg/m2 (SD, 5.5 kg/m2). Median serum 25(OH)D level was 92 nmol/L (interquartile range, 74–118 nmol/L). Using cut-offs of < 25 nmol/L for deficiency and < 50 nmol/L for insufficiency, two women were vitamin D deficient (one was Middle Eastern and one was South-East Asian) and five women were vitamin D insufficient (three were white, with lowest serum 25[OH]D level of 40 nmol/L, and two were Indian Subcontinental). The result of a Fisher exact test suggested an association with ethnicity (P = 0.01). A χ2 value of 21.36 (P < 0.001) confirmed that the proportions of deficiency and insufficiency in our study population were significantly different to those of Lau et al’s study population. The majority of serum samples (40) were obtained in winter, followed by spring (21), summer (10) and autumn (three). Six of the seven results of deficiency and insufficiency were from samples obtained in winter; the other was from a sample obtained in September. Excluding autumn, categorical and continuous analyses showed borderline significant variation of 25(OH)D level by season (Mann–Whitney U test [P = 0.08] and Kruskal–Wallis test [P = 0.08], respectively). Several factors may account for the difference in vitamin D deficiency and insufficiency prevalence between our study and that of Lau et al. The most obvious is the “Sunshine State” factor, because several studies in southern states have reported higher prevalence of vitamin D insufficiency than in our study.3-5 In Lau et al’s study, a large proportion of women were at high risk of vitamin D deficiency (only 19% were white) and the women were recruited from a gestational diabetes mellitus clinic. Care should be taken in extrapolating such findings to the wider population. Although our study was not population based, it included a majority white and healthy general obstetric population, rather than sampling at a clinic where women are at high risk of vitamin D insufficiency. We are not asserting that gestational vitamin D levels are unimportant. The increasing incidence of rickets in Australia,2 along with other potential hazards, dictate that increased awareness is mandatory. However, as opposed to routine screening in all pregnancies, our data suggest that local assessment of vitamin D status and demographic risk factors (in gestational diabetes mellitus and general obstetric populations) should be the priority.

Donald S A McLeod · Katherine A Scott · Karin M C Lust · H David McIntyre

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