Inappropriate use of dual energy absorptiometry body composition estimation

To the Editor: Bone densitometry by means of dual energy absorptiometry (DXA) has been the gold standard for estimating bone mineral density (BMD) for over 3 decades and is pivotal in the current management of osteoporosis. DXA technology relies on measuring the attenuation of two different x-ray energies that can be used to calculate BMD or, alternatively, soft tissue mass, including fat and lean tissue mass. Over the past few years, there has been increasing use of DXA for estimating fat and lean tissue in body composition. These parameters are widely used in research into diseases that affect body composition (such as HIV, obesity and eating disorders), and increasingly in related clinical settings. While using DXA in this way is beneficial in some patients, there is anecdotal evidence of growing inappropriate use or overuse of DXA body composition estimation in monitoring weight loss or exercise programs, often supplied by non-medical practitioners.

Two problems are worth highlighting. First, a number of body composition scan providers imply that total body BMD, provided automatically with the whole body composition scans, can provide a diagnosis of osteoporosis. This is inconsistent with World Health Organization guidelines of osteoporosis being indicated by a T score for bone density that is 2.5 SD or more below the young adult mean, which applies only to the lumbar spine, proximal femur and mid shaft radius but does not apply to total body BMD.1 Applying the criterion of T ≤ − 2.5 SD to the whole body BMD, as provided by body composition scans, will underestimate the prevalence of osteoporosis.2

Second, some providers recommend that DXA for estimating body composition be performed 3-monthly. Although DXA for estimating body composition delivers a low radiation dose, the radiation safety principle of ALARA (As Low As Reasonably Achievable) should always be followed and there is no published evidence supporting this scan frequency. Unfortunately as DXA for estimating body composition falls outside Medicare, the federal government has no incentive to act. Moreover the low radiation dose from DXA results in relatively little attention from state radiation regulators.

First Australian report of vitamin D-dependent rickets type I

A 20-month-old girl presented to hospital with features of rickets. Results of investigations were consistent with vitamin D-dependent rickets type I (VDDR-I), and DNA sequence analysis showed a homozygous mutation in the CYP27B1 gene of c.1325-1326insCCCACCC. This is the first reported Australian case of VDDR-I.

Clinical record

A 20-month-old white Australian girl presented to the Women’s and Children’s Hospital in Adelaide, South Australia, with a 6-month history of developmental regression of gross motor skills, failure to thrive and irritability, in particular distress when “she was wearing her shoes”. At 14 months of age, she had been crawling, pulling to stand and cruising, but at presentation her gross motor skills had regressed to only being able to sit unsupported. Other developmental milestones continued to progress normally for her age. Her weight at presentation was 7.7 kg, having dropped from the 50th centile to below the third centile (weight loss of 3.7 kg over 6 months). Length and head circumference had dropped from the 25th centile to less than the first centile and to the third centile, respectively, over this time.

The patient was the second child born to non-consanguineous white Australian parents. She was born at term with no perinatal complications. There was no history of familial hereditary disease. Maternal vitamin D deficiency had been treated during the pregnancy. The patient had received a multivitamin supplement (0.45 mL/day of Penta-vite [Bayer Australia], containing 10.1 µg of cholecalciferol) from birth until 2 months of age, with no further follow-up until her presentation at 20 months (Box 1).

On examination, the patient was mildly dehydrated, listless, miserable and mildly tachypnoeic, with intercostal recession. Her anterior fontanelle was large. Rachitic rosary, tibial bowing and widened metaphyses of the wrists and knees were evident. No bruising of the skin was noted.

The patient had low serum total calcium and inorganic phosphate levels and a markedly elevated alkaline phosphatase level (Box 1). A skeletal survey showed significantly osteopenic bones, with flaring of the metaphyses in the long bones, soft tissue swelling around the elbow and wrist joints, and steep acetabular angles (Box 2). She had acute and healed fractures in multiple places: the right proximal ulnar shaft; both distal radial shafts; mid shafts of the second, third and fourth metacarpals of the right hand; mid shaft of the second metacarpal of the left hand; and mid shafts of the third metatarsals of both feet.

The clinical, radiological and biochemical findings were consistent with a diagnosis of rickets. She was treated with two doses of intravenous calcium infusion (12.5 mL/day of 10% calcium gluconate), oral phosphate (100 mg/kg/day) for 4 days, oral calcium (75 mg/kg/day) for 5 months, and ongoing calcitriol (0.07 µg/kg/day). She had feeding problems (food refusal and difficulty swallowing), which required nasogastric feedings for a month and a high-calorie diet.

The differential diagnosis included nutritional vitamin D-deficient rickets, vitamin D-dependent rickets (VDDR) type I and II, and hypophosphataemic rickets such as X-linked hypophosphataemia (Appendix 1). In the presence of normal renal function, electrolyte levels and acid–base balance, in addition to a low 1,25-dihydroxyvitamin D (1,25(OH)2D) level, normal 25-hydroxyvitamin D (25(OH)D) level, high alkaline phosphatase and parathyroid hormone (PTH) levels, and hypocalcaemia, the most likely diagnosis was VDDR type I (VDDR-I).

As VDDR-I is caused by a mutation in the CYP27B1 gene that impairs the conversion of 25(OH)D to 1,25(OH)2D, gene sequence analysis of the CYP27B1 gene was undertaken using genomic DNA from the index patient and her parents. All nine exons and intron–exon boundaries of CYP27B1 were amplified by polymerase chain reaction (PCR) from 100 ng of genomic DNA, using the PCR primer sets published previously.1 PCR conditions were 94°C for 5 min, followed by 35 cycles of amplification (94°C for 30 s, 54°C for 30 s, and 72°C for 30 s). The resulting PCR products were directly sequenced using Applied Biosystems 3730 and 3730xl DNA analysers. A biallelic c.1325-1326insCCCACCC sequence variation was found in exon 8 of the CYP27B1 gene (Appendix 2), which in turn led to a frameshift mutation and premature stop codon after 23 altered amino acids (F443PfsX466 or F443fs). As expected, a monoallelic c.1325-1326insCCCACCC sequence variation was found in both parents (Appendix 2). The parents have been counselled regarding their genetic status and the risk of having another child affected in an autosomal recessive manner.

Sixteen months after discharge, at 3 years of age, the patient demonstrated good catch-up in weight (12.6 kg; 10–25th centile), with a growth velocity of 7.8 cm/year (25–50th centile). She was walking unaided and walking up and down stairs. Metaphyseal widening and tibial bowing had decreased but were still present on clinical examination. She continued to receive calcitriol at a dose of 0.07 µg/kg/day, and her PTH, calcium and phosphate levels were within reference intervals (Box 1). A renal ultrasound produced normal results, with no evidence of nephrocalcinosis.

Discussion

We believe this is the first reported Australian case of VDDR-I with an identified mutation, demonstrated by a clinical presentation of severe rickets, severe hypophosphataemia, high PTH level, low 1,25(OH)2D level, failure to thrive and unresponsiveness to 25(OH)D therapy. The patient showed mild hypocalcaemia on admission due to the compensatory high PTH level. These findings are compatible with the current notion that the bone phenotype of rickets and osteomalacia mainly results from hypophosphataemia, not hypocalcaemia. Independent hypocalcaemia will not cause rickets or osteomalacia in hypoparathyroid patients, while hypophosphataemia alone causes rickets and osteomalacia in fibroblast growth factor 23 (FGF23)-related hypophosphataemia.2 The mutation of CYP27B1 in this case, c.1325-1326insCCCACCC, has been reported previously in diverse ethnic groups (Appendix 3).3–9 The final aberrant CYP27B1 protein lacks 44 amino acids in the C-terminus, resulting in reduced or no enzymatic activity to convert 25(OH)D into 1,25(OH)2D. This is the most common mutation among patients with VDDR-I; of 67 families with VDDR-I reported in the literature, including this one, 20 harbour this mutation. The index case is the first reported VDDR-I mutation in the Australian population, but ethnicity is irrelevant to the frequency or phenotype of the disease.

Previously described patients with VDDR-I have presented around the same age, with similar features (failure to thrive and regression in gross motor development) and similar results of biochemical investigations. Clinical data on the frequency of fractures in VDDR-I patients are limited due to the rarity of the disease.3–9 As there were no other causes found for the multiple fractures seen in our patient, these might have been related to the delay in diagnosis and treatment in a child who was increasing in mobility due to developmental progression. Almost all reported patients with VDDR-I have required regular calcitriol treatment. Although the required dose of calcitriol may depend on each patient, generally a dose of 0.01–0.1 µg/kg/day normalises serum calcium and inorganic phosphate levels in patients with VDDR-I.10

1 Results of laboratory investigations and calcitriol dose at each available time point

		Patient’s age
Variable	RI	1 day	3 days	2 months	20 months (admission)	21 months (discharge)	25 months	29 months	32 months	34 months	37 months

Total calcium (mmol/L)	2.10–2.65	—	—	2.36	2.00	2.32	2.20	2.33	2.31	2.32	2.21
Inorganic phosphate (mmol/L)	1.15–2.50	—	—	1.04	0.75	0.70	1.09	0.86	0.75	1.94	1.71
Alkaline phosphatase (U/L)	100–360	—	—	1078	3848	1494	969	1322	953	467	276
Parathyroid hormone (pmol/L)	0.5–5.5	—	—	32.9	37.0	33.1	15.2	29	14.8	3.7	2.3
25(OH)D (nmol/L)	> 60	63	48	89	62	—	—	—	—	—	—
1,25(OH)2D (pmol/L)	50–160	—	—	—	17	—	—	—	—	—	—
Calcitriol dose (µg/kg/day)	na	—	—	—	0.01–0.04	0.07	0.07	0.07	0.07	0.07	0.07

RI = reference interval. na = not applicable. — = data not available. 25(OH)D = 25-hydroxyvitamin D. 1,25(OH)2D = 1,25-dihydroxyvitamin D.

2 X-ray at presentation demonstrating rachitic changes

No need to be wary of dairy, study finds

A small daily serve of milk or cheese can reduce the risk of heart disease and stroke even among people who have not traditionally eaten dairy products, a long-term study has found.

In a result that undermines fears in some Asian countries that adding milk and cheese to traditional diets is contributing to a jump in heart attacks, strokes and cancer, Monash University researchers found that eating a little dairy most days actually improved health.

“In a dominantly Chinese food culture, unaccustomed to dairy foods, consuming them up to seven times a week does not increase mortality and may have favourable effects on stroke,” lead author Emeritus Professor Mark Wahlqvist said. “We observed that increased dairy consumption meant lower risks of mortality from cardiovascular disease, especially stroke, but found no significant association with the risk of cancer.”

Lactose intolerance is particularly common in Asia – in some countries it can be as high as 90 per cent – helping fuel resistance to including dairy products in the diet.

But the study, which began in 1993 and has involved tracking the eating habits and health of 4000 Taiwanese, found that consuming even small amounts of milk, cheese or yoghurt could improve health.

Professor Wahlqvist said those who ate no dairy products actually had higher blood pressure, body fat and body mass indices than those who did.

“Taiwanese who included dairy food in their diet only three to seven times a week were more likely to survive than those who ate none,” he said, adding that people only needed to eat small amounts to gain a benefit.

The key is daily consumption of dairy foods, at the rate of about five servings (the equivalent of about five cups of milk or 225 grams of cheese) spread over a week, the study found.

Such quantities rarely cause problems, even for people considered to be lactose intolerant, Professor Wahlqvist said.

The study, which also involved researchers from the National Health Research Institutes and National Defence Medical Centre in Taiwan, was published in the Journal of the American College of Nutrition.

Adrian Rollins

Weight loss options in general practice

A positive approach, using the 5As, is required when helping obese patients manage their weight

Obesity, defined as a body mass index (BMI) of 30 kg/m2 or more, is increasingly prevalent in Australia, affecting 28% of adults, 7% of children aged 5–17 years and 27% of patients who present to general practice.1,2 Overweight and obesity are strong risk factors for chronic conditions such as diabetes, which have also been steadily increasing over the past two decades.1 Although obesity is ultimately due to an imbalance between energy intake (diet) and expenditure (digestion, metabolism and physical activity), this is influenced by a complex range of other factors, including genetics, epigenetics, the gut biome, the social environment, culture and health literacy over the life cycle.3

In the face of this complexity and repeated failed efforts by their patients to lose weight, many clinicians feel frustrated, attributing the lack of success to lack of patient motivation.4 The negative attitudes of some clinicians, in turn, result in many patients trying to lose weight without medical support.5 Yet, obesity can be addressed successfully and even small amounts of weight loss are associated with lowered cardiovascular risk and delayed onset of chronic conditions such as diabetes.3

The 5As approach provides a useful framework for general practitioners to help obese patients manage their weight and was adopted in the recent National Health and Medical Research Council (NHMRC) clinical management guidelines.3 It involves the following steps:

ask and assess BMI, waist circumference, diet (especially fruit, vegetable and fat intake), physical activity, comorbidities, medications that might contribute to weight gain, and readiness to change
advise on the benefits of a healthy lifestyle and weight management; even small amounts of weight loss (5%) are beneficial
assist by providing (directly or by referral) education on diet, physical activity and behaviour change; a diet that produces an energy deficit of 2500 kJ per day and 300 minutes of moderate-intensity activity or 150 minutes of vigorous activity per week are recommended
- if BMI > 30 kg/m2 with no weight loss, consider a very low energy diet
- if BMI > 40 kg/m2 or > 35 kg/m2 with comorbidities, consider surgery
arrange follow-up and review, to prevent relapse and provide support.

Effective interventions target both diet and physical activity, use established behaviour-change techniques and mobilise social support.6 Fad diets are unhelpful. Low-carbohydrate, high-protein diets can be useful in achieving short-term weight loss but caution is needed because there is evidence of increased long-term cardiovascular risk.7 Very low energy diets using meal replacements can be beneficial but require careful monitoring and support (although meal replacement products are available without a prescription).

Obese patients are not often referred to allied health professionals (eg, dietitians, exercise physiologists and health educators), even though such referrals can help patients achieve and maintain modest weight loss. Education and coaching in diet and physical activity change has been shown to result in 3%–10% weight loss.8,9 There are many different weight loss services and programs run by commercial providers, health clinics, government agencies and non-government organisations. However, not all are evidence based and it can be a challenge for GPs to know which will be effective. Further, many patients fall by the wayside because of cost, availability, transport, and appropriateness for their language, sex or cultural background. Cost can be reduced by using chronic disease management items in the Medicare Benefits Schedule when referring patients who have chronic conditions; these help patients access multidisciplinary care from three providers. It is important to assist patients as they navigate the complexities of the health care system, especially patients with low health literacy.

Currently available medications are not well tolerated and have limited effectiveness in weight maintenance. Orlistat and phentermine are the only weight loss drugs registered for use in Australia. Both are expensive and neither is listed on the Pharmaceutical Benefits Scheme. In this issue of the Journal, Neoh and colleagues10 show that a combination of phentermine and topiramate is poorly tolerated due to adverse effects. A phentermine–topiramate combination was recently approved for use in the United States, although the approved formulation and doses differed from those used in Neoh et al’s study.

Another article in this issue, by Lukas and colleagues,11 adds to the body of evidence showing that surgery is effective in not only achieving weight loss but also in control of comorbidities, especially diabetes.12 The choice of surgical procedure (eg, laparoscopic adjustable gastric banding, laparoscopic sleeve gastrectomy or Roux-en-Y bypass) should be individualised. Surgery should not be considered a last resort, especially because relatively young patients can benefit. However, surgery is an expensive option for most people (as access to bariatric procedures in the public sector is limited, despite evidence of effectiveness), and surgery is most effective when it is part of a multidisciplinary approach that includes diet, physical activity and psychological support.

Whatever the treatment approach, follow-up is important. This should be frequent: fortnightly for the first 3 months of a weight loss program with review and escalation in intensity if there is less than 1% decrease in weight.

It is not news to GPs that there is no panacea to the obesity epidemic and that other interventions are required early in life and at a population level. However, there is justification for some optimism — modest weight loss and reductions in health risk are possible, and GPs have an important role to play in helping patients manage their weight.

The efficacy of bariatric surgery performed in the public sector for obese patients with comorbid conditions

Obesity (body mass index [BMI] ≥ 30 kg/m2) is a growing health problem and is recognised as one of the largest contributors to the chronic burden of disease. Currently, 28% of Australians are obese, placing our nation second for men and fifth for women among OECD (Organisation for Economic Co-operation and Development) countries ranked by prevalence of obesity.1,2 In Australia, an inverse relationship exists between high obesity prevalence and low socioeconomic status; incidence is almost double for areas indexed as the most disadvantaged compared with areas within the highest strata.3 Those living more remotely also have higher obesity rates — 59% versus 32%.2 Among Indigenous Australians, the prevalence of obesity is almost double (34% versus 18%) and that of type 2 diabetes mellitus (T2DM) is triple that of non-Indigenous adults, resulting in sevenfold greater mortality due to diabetes.2,4

Bariatric surgery is an effective treatment of severe obesity (class III [BMI ≥ 40 kg/m2] or class II [BMI ≥ 35 kg/m2] with comorbid conditions) and is purportedly cost-effective, compared with conservative measures.5–7 The evidence supports sustained postoperative weight loss, ameliorating obesity-related comorbid conditions. The Swedish Obesity Study showed a marked reduction in hypertriglyceridaemia, T2DM and hyperuricaemia with surgery after 2 and 10 years.6 The resultant postsurgical weight loss substantially reduces, resolves and even prevents the metabolic complications associated with increasing central adiposity, with 73%–95% T2DM remission rates by 2 years, depending on the type of surgery.8,9

The heavy economic burden of obesity and its comorbid conditions may be alleviated in the long term by surgical management, despite upfront resource costs.10 Severely obese individuals incur twofold higher mean annual health care costs ($2788 v $1472) and use double the number of medications annually (11.4 v 5.3 per person) compared with the general population.7,11 Weight loss surgery can reduce the number of medications required and lower individual health care costs by 26%, a direct saving of $506 per person.7,12 With evidence of reduced mortality and an acceptably low complication profile (estimated mean 30-day mortality < 0.3%), bariatric procedures are supported by national and international health bodies.13–15

The National Health and Medical Research Council (NHMRC) 2013 guidelines recommend bariatric surgery as the most beneficial and cost-effective management for motivated individuals with severe obesity.16 Motivation is an essential factor in considering whether an individual with obesity and comorbid conditions is a suitable candidate for surgery. Surgery is not the final step in the clinical pathway of severe obesity management; postoperative commitment to lifestyle change and regular follow-up are requisite for successful weight loss and continued improvement in health.16 Most individuals are motivated to have surgery for greater control of medical ailments, yet it is unknown whether this applies to those whose procedure is fully funded.17

Since 1992, Medicare has reimbursed the cost of bariatric surgery in the private sector. As most surgery is carried out in private hospitals with large out-of-pocket expenses for those without private health insurance, a significant inequity in obesity management exists.18 Paradoxically, this surgery is least accessible to those who are likely to be in greatest need. Since October 2009, a pilot program has been underway in the Sydney and South Western Sydney Local Health Districts in which bariatric surgery has been publicly funded for a limited number of patients meeting strict inclusion criteria. There are no Australian studies to date that have identified if publicly funded surgical intervention for severe obesity confers the same health benefits seen in private health care. This study aims to assess the efficacy of bariatric surgery for such patients in the Australian public health system.

Methods

Study design

Sixty-eight moderately to severely obese participants with comorbid conditions were deemed eligible for bariatric surgery, and inclusion in our study. Participants were attendees at an ongoing collaborative pilot program run by one of three obesity clinics based within the Sydney and South Western Sydney Local Health Districts. All participants received conservative management for their obesity and related health conditions delivered by a multidisciplinary team trained in obesity management. Participants were seen 6- to 12-weekly for dietary advice, behavioural modification, advice on physical activity and, where appropriate, very low energy diets (VLEDs) and pharmacotherapy. Participants with substantial obesity-related comorbid conditions who had not achieved adequate weight reduction with conservative intervention, and who were interested in surgical management, were assessed by their multidisciplinary team to determine suitability for bariatric surgery. Longitudinal data were collected on those individuals who underwent bariatric surgery for management of resistant obesity and associated comorbid conditions.

The inclusion criteria for bariatric surgery were: age 18–75 years, minimum class II obesity (BMI ≥ 35 kg/m2) with comorbid conditions, completion of at least 1 year of medical intervention during which the participant had demonstrated commitment to lifestyle change, and surgery before 31 May 2013 (enabling a minimum follow-up period of 3 months). Exclusion criteria were: inability to consent, irreversible endocrine causes of obesity and significant comorbid conditions that were expected to result in poor outcomes from surgery, such as unstable cardiovascular disease and uncontrolled psychiatric illness. Participants underwent 2 weeks of VLED before the surgery to reduce abdominal adiposity and liver volume in particular, as liver size can complicate surgical access.19 They were also instructed about the necessary commitment to postoperative care, specifically the importance of nutritional input. Two of us (C J T and D J M) performed either laparoscopic sleeve gastrectomy (LSG) or laparoscopic adjustable gastric banding (LAGB) at a single public hospital. The type of surgery performed was decided by the participant in conjunction with the surgeon, after being briefed on the techniques, risks and expected benefits of each procedure. All participants were screened for nutritional deficiencies before and after surgery.

Ethics approval was obtained from four Human Research Ethics Committees within the Sydney and South Western Sydney Local Health Districts. All participants gave written consent for use of their records for research purposes.

Clincial and biochemical assessments

Surgeries were performed on an as-needed basis from 1 October 2009 to 31 May 2013. Pre- and postoperative results were analysed at seven time points until 1 September 2013. The baseline (preoperative) measurements were recorded at the start of the VLED, at least 2 weeks before surgery (time zero). Postoperative data were recorded from follow-up appointments at 3, 6, 12, 18, 24 and 36 months. The primary end points analysed were weight, BMI and waist circumference, and secondary end points were four common obesity-related comorbid conditions: T2DM, dyslipidaemia, hypertension (HTN), and obstructive sleep apnoea (OSA). Improvement was defined by normalisation of laboratory markers (T2DM and dyslipidaemia), blood pressure sphygmomanometry (HTN) and polysomnography results (OSA). Comorbid conditions were considered “partially resolved” when participants’ measurements fell within normal limits, the number of medications was reduced or the use of the continuous positive airway pressure (CPAP) device was discontinued. Comorbid conditions were deemed “fully resolved” when normal measurements remained after all relevant medications were discontinued.

Definition of comorbid conditions

T2DM was defined as fasting blood glucose levels ≥ 7 mmol/L, glycated haemoglobin level ≥ 6.5% and/or requirement of at least one oral hypoglycaemic agent. HTN was defined as systolic blood pressure ≥ 140 mmHg, diastolic blood pressure ≥ 90 mmHg and/or requirement of at least one antihypertensive agent. Dyslipidaemia was defined as total cholesterol level ≥ 5.0 mmol/L, low-density lipoprotein level ≥ 3.5 mmol/L, triglyceride level ≥ 2.0 mmol/L, or high-density lipoprotein level ≤ 1.01 mmol/L for men and ≤ 1.3 mmol/L for women, and/or requirement of at least one lipid-lowering medication.20,21 OSA was defined according to symptoms (snoring, observed apnoea, daytime somnolence), treated HTN and the apnoea–hypopnoea index record from polysomnography.

Statistical analysis

The results at the seven time points were reported as mean and SD. The differences were tested for significance using paired t tests for continuous variables and the McNemar test for paired categorical variables. The t test was used to evaluate between-surgery differences in mean weight at baseline and subsequent time points, to assess the validity of combining the two surgery types in analyses. Mixed-model regression was used to determine if significant change in weight occurred over time at all seven time points, to account for reductions in sample size with time. All statistical analysis was performed using SAS version 9.3 for Windows (SAS Institute).

Results

Participant characteristics

Of the 68 participants offered surgery, two declined and one moved interstate. Sixty-five participants (41 women and 24 men) with a mean age of 51.5 years (SD, 11.8 years; range, 21–73 years) underwent bariatric surgery between 1 October 2009 and 31 May 2013. The level of comorbid conditions in the group at baseline was high, with a mean of eight conditions per patient and class III (severe) obesity. From baseline to 18 months, only three participants were lost to follow-up at each time point; however, numbers are lower with time as operations were done at different times (ie, only 10 patients had surgery 36 months ago whereas 65 had surgery 3 months ago, 58 had surgery 6 months ago, etc [see Box 1]). Data on all participants who completed follow-up at each respective time point according to surgery date are presented in Box 1 and Box 2.

Intraoperative outcomes

All 65 surgeries were performed laparoscopically and none required conversion to open surgery. The most commonly performed procedure was LSG (57 patients; versus eight patients who had LAGB). Despite it appearing that greater weight change occurred in the LSG group, the difference was not significant at 3 months (P = 0.58), 12 months (P = 0.25) or 24 months (P = 0.17). There were no significant intraoperative complications (one participant had a haematoma that resolved with immediate evacuation) and length of hospital stay was within expected times for all patients (LSG, three nights; LAGB, one night).

Short-term postsurgical outcomes (3–6 months)

There was a reduction in all primary end points in the early postoperative period. By 3 months there was a mean weight reduction of 22.6 kg (SD, 9.5 kg) (Box 3) with a 7.4 kg/m2 mean reduction in BMI and 14.5 cm mean reduction in waist circumference (Box 1). All comorbid conditions showed partial resolution from 3 months (Box 2). Of the numbers of participants who had each comorbid condition at baseline and who had data available, there was full resolution by 6 months in 20/45 with T2DM, 14/43 with HTN, 7/47 with dyslipidaemia and 17/41 with OSA (Box 2). The requirement for all relevant medications also reduced accordingly (Box 4).

Medium-term postsurgical outcomes (12–18 months)

By 1 year, there was a significant reduction in all anthropometric measures. The mean weight loss was 34.2 kg (SD, 20.1 kg), and the mean BMI was reduced by 12 kg/m2 to 36.2 kg/m2 (SD, 7.7 kg/m2). By 18 months, of those who reported the respective comorbid conditions at baseline, almost half of the group had full remission of T2DM and three-quarters had resolution of OSA. Modest resolution of dyslipidaemia was seen with both a significant rise in high-density lipoprotein and reduction in triglycerides occurring transiently at 6–12 months in 7 of 47 patients who had dyslipidaemia at baseline (P < 0.001).

Long-term postsurgical outcomes (24–36 months)

The trend for continued weight loss and partial or full resolution of comorbid conditions appears maximal at 12–24 months. While the smaller group sizes at the 24- and 36-month follow-ups provided less power for statistical analysis, primary and secondary end points remained stable (P < 0.001). The maximal amount of mean weight loss occurred at 24 months (39.9 kg; SD, 31.4 kg). Three-quarters of the cohort had reduced the number of medications taken for HTN and T2DM by 18–24 months, and by 36 months, all had reduced the number of antihypertensive medications (Box 4).

Postoperative complications

Transient nutritional deficiencies were found in three of 65 participants, improving within 3 months with replacement treatment. Of the eight patients who had LAGB, one underwent conversion, due to gastric band erosion, to a Roux-en-Y bypass at 18 months. Of the participants who had LSG, one had a small bowel obstruction secondary to adhesions and required laparoscopic division at 2 years. Three participants required endoscopic stomach dilatation and a further three continued to experience nausea, dyspepsia and/or vomiting at 3 months, but this resolved by 6 months for two and at 12 months for one participant.

Weight change over time

A total of 288 observations for weight from 65 participants were available for linear mixed-model analysis. Significant change in mean weight was observed over time (P < 0.001). Mean weight adjusted for baseline weight decreased from 136.5 kg at baseline to 101.1 kg at 12 months. Stratifying the analysis by sex showed that men had a higher mean baseline weight, 147.5 kg (SD, 36.9 kg) compared with women, 130.1 kg (SD, 23.8 kg), but no difference was observed after 1 year (Box 3).

Discussion

In our study, the significant weight lost by obese participants who underwent bariatric surgery occurred early and was sustained over the first 3 years. The mean maximal weight loss was almost one-third of participants’ preoperative weight and was achieved by 24 months. Despite decreasing sample sizes, our results showed sustained weight loss at 36 months.

There was full or partial resolution of all comorbid conditions tested, except dyslipidaemia, in most participants by 2 years. Different rates of resolution of comorbid conditions occurred, with remission of T2DM being the earliest. By 24 months, there was an associated resolution of T2DM, HTN and OSA, or the need for pharmacotherapy or devices was reduced in most patients, yet dyslipidaemia showed inconclusive results. These findings parallel other bariatric studies.22,23 The Swedish Obesity Study found isolated improvements in hypertriglyceridaemia postoperatively (including after LAGB), although the most consistent improvements in lipid profiles have been seen after Roux-en-Y bypass surgery.6,24

Most LAGB procedures were performed in the first year of the study, until LSG became a preferred option due to its greater weight loss profile with minimal additional complications and the lower need for surgical follow-up. However, throughout the study, participants had autonomy of procedure choice (on surgeon recommendation). While this may suggest an avenue for bias (the participants chose their “intervention”), bariatric surgery is an elective procedure, and it was deemed necessary to replicate the protocol in the private sector. The limitations of our study include its small size, that it is a case series, that it is non-blinded, possible bias due to participants choosing their surgery type, and the use of a clinical database with the possibility of missing or inaccurate values imputed by health professionals. The low rates of adverse events observed in our study are consistent with those reported in the literature.

The direct operative costs of performing these surgeries in the public sector in our study were estimated to be $7000–$9000 (LSG incurred greater up-front theatre costs than LAGB). Perioperative costs, including 2 years of postsurgical visits, may approach $2000 per person, taking the total cost to $9000–$11 000 per person. A 2005 paper reported the annual cost of managing an individual with T2DM as $9095–$15 850.25 Thus, if an obese person with T2DM has bariatric surgery, the operation would pay for itself after about 1 year.

The participants’ baseline characteristics are representative of a typical demographic seen in the public sector, supporting extrapolation of our results to a wider population. The high attendance rate at 2 years shows that the cohort demonstrated adequate motivation to justify surgical intervention. The health potential from bariatric surgery ranges from improved quality of life and amelioration of comorbid conditions to full resolution of complications and reduced mortality for all individuals, paying or not. Strategies to prioritise access are therefore recommended to reduce the apparent inequality that exists. Limited access to surgery discriminates against those who cannot afford the out-of-pocket costs, yet it is likely that this subgroup would benefit most. In conclusion, we hope that our study provides an evidence base for the surgical treatment of obesity in the public health system and, in turn, that consideration will be given to increasing the supply of publicly funded bariatric surgery in Australia.

1 Patient anthropometric data before and after bariatric surgery

Measurement

Baseline (2 weeks before surgery)

Postoperative month 3

Postoperative month 6

Postoperative month 12

Postoperative month 18

Postoperative month 24

Postoperative month 36

N (n)

65 (65)

55 (58)

49 (52)

30 (33)

17 (23)

7 (10)

BMI (SD), kg/m2

48.2 (9.5)

40.8 (8.3)*

38.9 (7.9)*

36.2 (7.7)*

38.2 (12.1)*

35.7 (7.7)*

38.7 (9.4)†

Weight (SD), kg

136.5 (30.3)

113.9 (25.2)*

108.3 (24.8)*

101.1 (22.4)*

99.3 (20.8)*

97.6 (21.9)*

108.6 (25.6)†

Waist circumference (SD), cm

132.2 (16.5)

117.7 (15.2)*

114.9 (14.7)*

109.4 (13.7)*

110.2 (12.3)*

108.4 (15.8)*

114.9 (14.6)*

% weight loss from baseline

17%

21%

26%

27%

29%

21%

BMI = body mass index. N = total number of participants who attended follow-up. n = total number of participants including those lost to follow-up. * Comparison between baseline and follow-up; P < 0.001. † Comparison between baseline and follow-up; P < 0.05.

2 Proportions of patients* who continued to have conditions found at baseline

Comorbid condition

Baseline (2 weeks before surgery)

Postoperative month 3

Postoperative month 6

Postoperative month 12

Postoperative month 18

Postoperative month 24

Postoperative month 36

T2DM

36/52†

25/45†

21/42†

12/23†

8/17‡

3/6

HTN

45/51‡

29/43†

18/40†

10/27†

4/12‡

2/6‡

Dyslipidaemia

45/58‡

40/47

33/42

13/24‡

8/15‡

4/6

OSA

37/41

24/41‡

15/41†

6/24†

4/17‡

2/5

OSA requiring CPAP

18/27

14/23‡

8/22†

4/13‡

2/8‡

1/3

CPAP = continuous positive airway pressure. HTN = hypertension. OSA = obstructive sleep apnoea. T2DM = type 2 diabetes mellitus. * Numerators are number of participants who had that condition at that time point. Denominators are total number of participants who had that condition at baseline and had data at that time point. † Comparison between baseline and follow-up; P < 0.001. ‡ Comparison between baseline and follow-up; P < 0.05.

3 Patients’ weight change over time after bariatric surgery*

* Weight change at all seven time points is significant (P < 0.001). Despite differences in weight lost for men and women, there were no significant between-sex differences.

4 Number of patients with a reduction in medications used at each time point after bariatric surgery

	Antihypertensive medications		Glucose-lowering medications		Lipid-lowering medications
Postoperative month	Patients at each time point	Patients with reduced use of medication	Patients at each time point	Patients with reduced use of medication	Patients at each time point	Patients with reduced use of medication

3	65	31	60	28	64	6
6	54	34	54	29	53	10
12	48	37	47	25	44	12
18	29	22	23	17	24	12
24	16	12	16	15	13	3
36	6	6	6	4	4	1

Combination phentermine and topiramate for weight maintenance: the first Australian experience

The global obesity epidemic has not spared Australia; 62.8% of adults were classified as obese or overweight in the 2011–12 financial year.1 While bariatric surgery is effective, access is poor for those most in need.2 Calorie restriction diets are successful in inducing weight loss, but weight is usually regained with time owing to hormonal adaptations that increase hunger, which occur in response to weight loss.3 There is a clear role for pharmacotherapy in appetite suppression for maintenance of weight loss.

The US Food and Drug Administration recently approved combination phentermine and controlled-release topiramate (in doses ranging from 3.75 mg phentermine plus 23 mg topiramate to 15 mg phentermine plus 92 mg topiramate) for use in adults with a body mass index (BMI) > 30 kg/m2, or > 27 kg/m2 with at least one weight-related comorbidity. Phentermine is a sympathomimetic agent that induces serotonin, noradrenaline and dopamine reuptake inhibition, suppressing appetite. Topiramate causes weight loss;4 its postulated effects include increasing energy expenditure, decreasing energy efficiency and decreasing caloric intake. In Australia, phentermine is available for use as short-term monotherapy for obesity and topiramate is available for treatment of epilepsy, migraine prophylaxis and treatment of neuropathic pain.

The efficacy of phentermine–topiramate has been assessed in Phase III trials, with a maximal weight loss of 10.9% reported for overweight and obese patients.5–7 The most frequent adverse effects were dry mouth, paraesthesia, constipation and insomnia. Recent studies have shown that phentermine monotherapy is relatively safe; it has no significant effects on blood pressure and heart rate8 and it does not induce psychological dependence or addiction.9

Phentermine–topiramate therapy is used for maintenance of weight loss in selected adults who attend the Austin Health Weight Control Clinic, a tertiary centre obesity service. We aimed to investigate its safety, tolerability and efficacy.

Methods

Patients who attend the Austin Health Weight Control Clinic follow a ketogenic very low energy diet (VLED) to suppress hunger10 until they achieve a target weight. They then receive dietary advice on reintroduction of carbohydrates. Selected patients are also offered oral phentermine 15 mg and topiramate 25 mg (a non-controlled release formulation that is taken in the morning) for an indefinite period for maintenance of weight loss. Those who have active ischaemic heart disease or severe hypertension, and those who are concurrently taking antidepressants, are not offered pharmacotherapy. Women of childbearing age are counselled about the teratogenicity of topiramate, which causes cleft lip and palate in the fetus. Patients are seen monthly during the weight loss phase and at the physician’s discretion during the weight maintenance phase (usually 3-monthly).

We used the Austin Hospital’s pharmacy records to identify patients dispensed phentermine–topiramate between 22 January 2010 and 16 July 2012. Patient data (sex and age; weight, height and blood pressure measurements; and qualitative data regarding potential adverse effects and reasons for ceasing pharmacotherapy) were collected from the Weight Control Clinic’s electronic database. Data collection continued until July 2013. Patients who did not attend the clinic for more than 6 months were defined as being lost to follow-up.

We analysed the data at four time points: Time 1, the initial visit; Time 2, the end of the VLED; Time 3, the time point during pharmacotherapy at which the nadir weight measurement was taken; Time 4, the time point during pharmacotherapy at which the last weight measurement was taken. For those lost to follow-up, weight measurements at Time 1 were carried forward to calculate mean final weight and mean final BMI, an intention-to-treat analysis. For those who ceased pharmacotherapy before the end of the data collection period, we analysed mean weight 3–6 months and 12–18 months after cessation, using available weight data.

Statistical analysis was performed using SPSS Statistics 20.0 (IBM). Paired t tests were used to compare weight and blood pressure data between time points.

The Austin Health Research Ethics Unit approved the study as an audit activity.

Results

During the study period, 125 patients were dispensed phentermine–topiramate. Data for 103 patients were analysed as no data were available for the remainder. Patients were initially severely obese (Box 1), and the mean duration of pharmacotherapy was 10 months (median, 6 months; interquartile range, 13 months). Mean weight decreased by 13.0 kg due to the VLED, a 10% decrease. Mean weights at Time 3 and Time 4 were significantly lower than mean weights at Time 1 (P < 0.001). Using intention-to-treat analysis, mean final weight and mean final BMI (119.9 kg, 42.7 kg/m2) were significantly lower than mean weight at Time 1 and mean BMI at Time 1 (135.5 kg, 48.6 kg/m2), respectively (P < 0.001).

Pharmacotherapy was ceased by 61 patients (41 ceased due to adverse effects ascribed to pharmacotherapy, and 20 for other reasons [eg, three started antidepressant therapy, one was planning to get pregnant and one had laparoscopic banding]), 30 patients continued pharmacotherapy, and 12 patients were lost to follow-up.

A total of 67 adverse effects were reported among 52 patients, the most frequent being paraesthesia, cognitive changes and depression (adverse effects of topiramate) and headaches, dry mouth and palpitations (adverse effects of phentermine) (Box 2). There was a significant difference in mean systolic blood pressure between Times 1 and 3 (P = 0.02) but no significant differences for mean systolic or diastolic blood pressure between other time points (Box 3).

For the 30 patients who continued on phentermine–topiramate (Box 4), mean duration of pharmacotherapy was 22 months (median, 23 months; interquartile range, 12 months); 26 patients took it for > 12 months and 13 took it for > 24 months. Seven of these 30 patients had adverse events: dysgeusia, dry mouth, paraesthesia, agitation, nausea and, in one patient, initial memory loss. Between Times 1 and 2, mean weight for these patients decreased by 16.0 kg — a 12% decrease. By Time 4, overall, the mean weight decreased by a further 6.7 kg. However, for men, the decrease in weight between Time 2 and Time 4 was not significant. No significant changes were observed in blood pressure measurements for these patients (data not shown).

Weight data after ceasing pharmacotherapy were available for 51 patients who ceased pharmacotherapy (Box 5). Between Times 1 and 2, mean weight for these patients decreased by 11.4 kg. By the end of pharmacotherapy, the mean weight decreased by a further 3.8 kg. At 3–6 months after cessation, mean weight had increased by 3.5 kg (based on data for 49 patients). By 12–18 months after cessation, mean weight increased by a further 1.0 kg (based on data for 28 patients). Mean weights at and after cessation of pharmacotherapy were statistically different to mean weights at Time 1 but not statistically different to mean weights at Time 2.

Discussion

To our knowledge, this is the first study of phentermine–topiramate use for maintenance of weight loss in Australia. About 40% of patients ceased pharmacotherapy due to adverse effects, which is significantly higher than the 8%–16% dose-related adverse effect dropouts reported for a Phase III trial of controlled-release phentermine–topiramate.5 The profile of adverse effects in our study also differs; we saw higher rates of depression, anxiety and cognitive changes. This could be due to over-reporting, as patients in our study were asked about adverse effects at each visit and most new symptoms were ascribed to phentermine and/or topiramate. The lack of a dose titration schedule and the use of a non-controlled release formulation in our study may have also contributed to the higher than expected number of adverse effects ascribed to topiramate.

Limited data were available for patients who ceased phentermine–topiramate therapy. Mean weight at 12–18 months after cessation was not significantly different to weight at the end of the VLED, but was significantly lower than the initial weight. However, this result represents only 28 patients and a short duration of follow-up.

The major limitation of this study is the lack of a control arm. The most common reasons for patients not being offered pharmacotherapy were antidepressant use and active ischaemic heart disease. This meant that the patients who were not offered pharmacotherapy were not suitable as comparators.

Combination pharmacotherapy with phentermine and topiramate may soon be available in Australia. The results of our study show low tolerability. However, for those who are able to continue phentermine–topiramate, the combination appears to be efficacious not only for maintenance of weight loss but also for ongoing weight loss.

1 Characteristics of the total cohort, reported as mean (SD)

Men (n = 38)

Women (n = 65)

Total (n = 103)

Age, years

50 (14)

48 (13)

49 (13)

Body mass index at Time 1, kg/m2

49.8 (12.6)

47.9 (9.4)

48.6 (10.7)

Weight at Time 1, kg

147.1 (38.3)

128.7 (26.8)

135.5 (32.6)

Weight at Time 2, kg

131.4 (33.0)†

117.3 (26.5)†

122.5 (29.7)†

Weight at Time 3, kg

126.1 (33.6)†‡

108.4 (26.4)†‡

115.1 (30.4)†‡

Weight at Time 4, kg

128.3 (34.1)†‡

111.5 (25.9)†‡

117.7 (30.2)†‡

Final weight, kg*

130.9 (37.6)†§

113.4 (26.5)†‡

119.9 (32.0)†‡

Final body mass index, kg/m2*

43.3 (11.4)¶

42.3 (9.0)¶

42.7 (9.9)¶

* Weight at Time 1 was carried forward for patients who were lost to follow-up. † P < 0.001 for difference when compared to weight at Time 1. ‡ P = 0.01 for difference when compared to weight at Time 2. § P = 0.79 for difference when compared to weight at Time 2. ¶ P < 0.001 for difference when compared to body mass index at Time 1.

2 Frequency of adverse effects in the total cohort (n = 103)*

Adverse effect

No. of patients

Likely causative drug

Paraesthesia

Topiramate

Cognitive changes

Topiramate

Headaches

Phentermine

Dry mouth

Phentermine

Palpitations

Phentermine

Depression

Topiramate

Change in sleep pattern

Phentermine

Nausea

Topiramate

Dizziness

Topiramate

Anxiety

Phentermine

Dysgeusia

Topiramate

Drowsiness

Topiramate

Aggression / behavioural change

Phentermine

Urinary frequency

Phentermine or topiramate

Restless legs

Phentermine or topiramate

Hair loss

Phentermine or topiramate

Constipation

Phentermine or topiramate

Skin rash

Phentermine or topiramate

* Adverse effects were reported by 52 patients.

3 Mean systolic and diastolic blood pressure for the total cohort (n = 103)*

* Error bars indicate SEMs; P = 0.002 for difference between systolic blood pressure at Time 1 and Time 3; P > 0.05 for all other differences.

4 Characteristics of patients who were on pharmacotherapy until the end of the data collection period, reported as mean (SD)

Men (n = 12)

Women (n = 18)

Total (n = 30)

Age, years

52 (15)

52 (9)

52 (12)

Body mass index at Time 1, kg/m2

50.3 (15.3)

50.2 (10.1)

50.2 (12.3)

Weight at Time 1, kg

136.4 (40.3)

130.2 (22.5)

132.6 (30.4)

Weight at Time 2, kg

121.4 (26.9)*

113.3 (18.3)*

116.6 (22.1)*

Weight at Time 3, kg

113.3 (28.9)*†

100.4 (15.2)*†

105.6 (22.2)*†

Weight at Time 4, kg

117.4 (34.9)*‡

105.0 (14.5)*†

109.9 (25.0)*†

* P < 0.001 for differences when compared to weight at Time 1. † P < 0.001 for differences when compared to weight at Time 2. ‡ P = 0.23 for difference when compared to weight at Time 2.

5 Mean weights of patients who ceased pharmacotherapy before the end of the data collection period*

* Error bars indicate SEMs; data at Time 1, Time 2 and time of cessation represent 51 patients; data at 3–6 months after cessation represent 49 patients; data at 12–18 months after cessation represent 28 patients; P < 0.001 for differences between weight at Time 1 and all other time points; P = 0.58 for difference between weight at Time 2 and 3–6 months after cessation; P < 0.001 for difference between weight at Time 2 and at cessation; P = 0.79 for difference between weight at Time 2 and 12–18 months after cessation.

Real food, supplements help the elderly stay healthy

Malnutrition is common among the elderly, but dieticians now say that nutritional supplements could be the answer to improving weight, protein and energy intake in older Australians, helping to avoid illness and unnecessary hospital stays.

In research published in the latest edition of Australian Prescriber, accredited practising dietician Anne Schneyder examined ways of improving nourishment in older people at risk of malnutrition.

“Most elderly people eat far less than they did when they were younger, and their energy needs are lower, but the requirements for some nutrients, like protein, calcium and riboflavin are higher,” she says.

“This means that their food has to be more nutritious to meet their needs.”

Studies have shown that malnutrition in the elderly can result in significant illness, hospitalisation, the development of pressure ulcers, infection, an increase in falls and fractures, and even death. Unintentional weight loss can also result in a reduction in the ability to care for oneself, loss of mobility and independence, and a poorer quality of life.

The rates of malnutrition in older people living at home are estimated to be as high as 30 per cent, and in aged-care facilities can be as high as 70 per cent.

Ms Schneyder said that for people at risk of malnutrition, using real foods was the first step to improving nutrition.

“Eating small frequent meals and snacks between meals, increasing the nutrient density of meals by adding milk powder, grated cheese, margarine and cream, and having nourishing fluids like milk drinks, smoothies and juice are the main ways to boost protein, energy and nutrients,” she said.

But Ms Schneyder says studies have shown that sensible use of nutritional supplements can also help improve weight, protein and energy intake, and quality of life overall.

“There are a number of supplements to choose from, and the most commonly and readily available are milk based,” she said.

“Specialised supplements are also available for particular medical conditions such as kidney disease.”

Ms Schneyder said that using nutritional supplements could be a valuable addition to the diet for an older person who was malnourished or at risk, but warned supplements should not be used on their own without a comprehensive assessment from a dietician.

“Overall, a good strategy for improving malnourishment in the elderly is about increasing protein and energy intake from food, preserving the enjoyment of food, and importantly, maintaining quality of life.”

Debra Vermeer

Open letter to the Hon Tony Abbott MP

Dear Prime Minister,

We urge you to include human-induced climate change and its serious health consequences on the agenda for this year’s G20 meeting. The world community looks to high-income countries for a strong lead. Current climate trends, driven by global warming, threaten the basis of future economic prosperity, regional political stability and human health.

As concern rises in many countries, including increasing awareness of the risks to human health and safety, many G20 members are strengthening their commitment to substantive mitigation action. The new United States regulations limiting coal-fired power plant emissions are explicitly linked to the protection of health. Meanwhile, if Australia passes up opportunities for new energy technologies and efficiencies, we will forfeit gains in long-term economic security and fail to contribute fairly to reducing worldwide risks to human health.

There are serious risks from climate change to the health of populations everywhere — widely documented in national and international scientific assessments. The risks include, but extend well beyond, intensified heatwaves, floods, fires and the spread of disease-bearing mosquitoes. Regional food yields and hence child and adult nutrition are at risk. Water shortages threaten the quantity and quality of drinking water, hygiene and agriculture. Warming and acidification of oceans endanger marine food sources. Infections such as gastroenteritis increase with warming, as do levels of important hazardous air pollutants. Threats to rural and coastal assets and livelihoods will adversely affect mental health.

Adverse health outcomes related to climate change are already evident in many regions of the world. By mid century, serious health risks are likely to be widespread, particularly in vulnerable communities, including in Australia. Workloads and economic and logistical demands on the nation’s health system will also rise as these impacts increase.

Near-term cost savings from health gains resulting directly from emission-reducing actions could be substantial. For example, the savings from health gains due to reduced heat extremes and accompanying air pollution would greatly exceed those accruing to agriculture from the same reduction in exposure.

In the long run, the harm to human health from climate change is more than an avoidable burden of suffering, injury, illness and premature death. It signals that our mismanagement of the world’s climate and environment is weakening the foundations of health and longevity.

This issue warrants urgent consideration at the G20 meeting. The health of present and future generations is at risk from ongoing human-induced climate change.

What will it take to curb the rise in obesity?

Shifting a whole population towards a healthy weight requires action targeting the root causes of obesity

The headline finding from our 2003 paper was a 2.5-times increase in the prevalence of obesity since 1980, with 20.8% of Australian adults found to be obese. Reporting the national obesity prevalence for the first time since 1995, this paper was one of the key outcomes from the Australian Diabetes, Obesity and Lifestyle study (AusDiab).1 AusDiab was the first Australian national diabetes study; it showed an adult prevalence of diabetes of 7.4% and that of prediabetes (elevated blood glucose levels but below the cut-point for diabetes) at 16.4%.2 These figures meant that prevention of the twin epidemics of obesity and diabetes was placed very much on the national agenda. AusDiab went on to become a longitudinal study, with the follow-ups of the cohort at 5 and 12 years providing invaluable data for studying obesity, diabetes, prediabetes, hypertension and kidney disease in individuals as they age. The more than 200 papers now published using data from this study have played an important role in influencing national public health policy and action.

With the prevalence of obesity continuing to climb since the baseline AusDiab survey (28.3% in the 2011–12 National Health Survey3), it is becoming clear that the lifestyle change programs and medical interventions that are often successful in trials and for individuals are effectively individual sandbags against the flood of obesity. Successfully shifting a whole population towards a healthy weight is likely to also require action targeting some of the root causes of obesity. Our increasingly sedentary and inactive lifestyles in combination with an environment full of cheap, tasty, heavily marketed and energy-dense foods make us highly susceptible to weight gain. Although we are each responsible for our own behaviour, these environmental and cultural factors combine to effectively conspire against healthy choices.4 In addition, a focus on adult lifestyles, although important, ignores the increasing body of data suggesting that the genesis of adult obesity is biological and cultural factors operating very early in life.5

A promising next generation of environmental obesity prevention initiatives include the excellent work done to improve the school food environment in many countries (now championed in the United States by First Lady Michelle Obama6), whole-of-community interventions such as the Healthy Together Communities program in Victoria7 and excellent work by researchers,8 retailers9 and others10 to change the way food is marketed and sold. Obesity prevention in mothers and in infants11 and prevention of excess gestational weight gain are further promising approaches. The combination of initiatives such as these will hopefully mean that when the Journal celebrates another decade, we will also be finally able to celebrate a reduction in Australia’s obesity prevalence.

Indigenous health: radical hope or groundhog day?

Professor Ernest Hunter explains why learning from the past and investing strategically will have the best chance of success

In his book Radical hope: education and equality in Australia, Aboriginal lawyer, academic and land rights activist Noel Pearson contends:

Governments and their bureaucracies are informed by everything other than memory of what was done five years ago, ten years ago and eighteen years ago. Politics are remembered, policies are not.1

It also includes his 2004 Judith Wright Memorial Lecture, in which, reflecting on the political forces necessary to drive national change in Indigenous affairs, he notes:

it will take a prime minister in the mould of Tony Abbott to lead the nation to settle the “unfinished business” between settler Australians and the other people who are members of this nation: the Indigenous people.1

A decade on, Tony Abbott, as Prime Minister, delivered the Closing the Gap report.2 Having identified that his government’s new engagements will involve centralising responsibility for Commonwealth-funded programs in the Department of the Prime Minister and Cabinet, setting up the Prime Minister’s Indigenous Advisory Council and fostering linkages between bureaucrats, business and Indigenous leaders, he details mixed outcomes across four key areas — health, education, employment and safe communities. The outcomes were consistent with the Closing the Gap Clearinghouse report released a year earlier,3 which identified key high-level principles and practices characterising programs that worked: flexibility to meet local needs and contexts; community involvement and engagement; building trust and relationships; a well trained and resourced workforce; and continuity and coordination. Themes associated with less successful initiatives included: programs implemented in isolation; short-term funding and high staff turnover; lack of cultural safety; and inflexible program delivery. Similar issues emerged in a recent review of early childhood parenting, education and health intervention programs.4

Clinicians working in remote Australia will not be surprised. There have been health gains, but they are uneven: remote Indigenous Australia is clearly behind. Furthermore, it can be argued that for some conditions and in some areas the situation is worse despite significant clinical investments. For instance, when I began work as a psychiatrist in Cape York and the Torres Strait over 20 years ago, there were no mental health or substance misuse services. Now there are well over 100 workers across Queensland Health, Education Queensland, the Royal Flying Doctor Service, Medicare Locals, community-controlled services and Commonwealth-funded programs, plus contracted private clinicians. This does not include the dozens of residents trained variously in community and personal wellbeing, empowerment, mental health literacy, suicide prevention and more. Sadly, the situation in terms of mental illness is worse, probably reflecting both contemporary social contexts and delayed effects of neurodevelopmental adversity.5,6

Our understanding of the developmental determinants of chronic disease in Indigenous Australians has been evolving for more than half a century7 and there is accumulating evidence on childhood social factors increasing the risk of adult-onset mental disorders. For example, bereavement stress in mothers during the first years of life (particularly after suicide in the family) increases the risk of affective psychosis.8 Research on such topics involves controlling for potential confounders. In the real world of remote Indigenous communities, many children are exposed to serial adversity: pregnancies affected by high levels of stress; poor nutrition and inadequate antenatal care; prematurity; infant environmental instability and attachment difficulties; hospitalisation and other forms of separation from caregivers; bereavement stress; exposure to violence; early-onset substance misuse; and more. We can only presume that the consequences of such risk amplification will be substantial.

In 2006, soon after Pearson commended him, Tony Abbott called for a new form of “paternalism” that would be “based on competence rather than race” to address unrelenting Indigenous health problems associated with failed past policies such as self-determination.9 Now, he holds the reins. But whatever happens, the economic agenda will weigh heavily; Indigenous Australians will not be quarantined from budget cuts, changes to Medicare and welfare entitlements, privatisation, and the continuing feud between federal and state governments over health funding. In Queensland, public sector services (particularly population health and health promotion) sustained dramatic losses in the 2012–13 financial year that will be most consequential for remote Indigenous communities. Career public sector employees are giving way to locums, casual workers, agency nurses and project workers funded by non-government organisations. While this may bring new ideas, it risks losing domain knowledge and incremental improvement based on practice-based evidence.10

While there is no doubt that greater economic self-reliance will be critical to Indigenous futures, I believe that there is complacency regarding the flow-on effects of the contraction of federal and state public sectors for Indigenous health in remote Australia. Indeed, to support self-reliance in the long term, it is critical that we increase and sustain strategic investment in public health and clinical programs for pregnancy and early childhood to optimise neurodevelopmental potential. Is it “radical hope” to suppose that the new paternalism and new engagements will deliver? Or, as Pearson suggests in his chapter on cycles of policy reinvention in Indigenous affairs, will it be groundhog day?