Subscribe
×

Preference: Indigenous Health

1

Reports indicate that changes are needed to close the gap for Indigenous health

Major changes in health services are needed to redress health disparities

Two recently released reports from the Australian Institute of Health and Welfare (AIHW) make it clear that there must be major changes in the way health services for Indigenous Australians are delivered and funded if we are to improve Indigenous health and health care and ensure real returns on the substantial investments that are being made.1,2

These reports show Australia’s level of financial commitment to Indigenous health. In the 2010–11 financial year total spending on Indigenous health was $4.552 billion,1 almost double that spent in 2004–05. This was $7995 for every Indigenous Australian, compared with $5437 for every non-Indigenous Australian;1 over 90% of this funding came from governments. The surest sign that this money was not well invested in prevention, early intervention and community services is that most of it (on average $3266 per person but $4779 per person in remote areas) was spent on services for patients admitted to hospitals, while spending on Medicare services and medicines subsidised by the Pharmaceutical Benefits Scheme (PBS) on a per-person basis was less than that for non-Indigenous Australians by $198 and $137, respectively.2

The series of AIHW reports since the 1995–96 financial year highlights both where progress has been made and where programs have failed. There have been considerable increases in funding for primary care, acute care and community and public health. The 2010–11 data do not reflect the full implementation of the Indigenous Chronic Disease Health Package, but do suggest that the measure to subsidise PBS copayments for patients with chronic disease is having an effect, specifically in more remote areas where PBS spending is higher than in regional areas.

On the other hand, it is obvious that access to primary care services in remote areas remains limited, and access to referred services such as specialists and diagnostics is poor for Indigenous people everywhere, even in major cities. Per-person spending on non-hospital secondary services is about 57% of that for non-Indigenous people.2 Indigenous Australians receive nearly all their secondary care in hospitals.

The hospital data hammer the story home. In 2010–11, the overall age-standardised separation rate of 911 per 1000 for Indigenous people was 2.5 times that for non-Indigenous people; for people living in the Northern Territory the rate was 7.9 times that for non-Indigenous people.3

About 80% of the difference between these rates was accounted for by separations for Indigenous people admitted for renal dialysis, but further examination highlights how a lack of primary care and prevention services drives increased hospital costs. In 2010–11, total expenditure on potentially preventable hospitalisations for Indigenous Australians was $219 million or $385 per person, compared with $174 per non-Indigenous Australian.3 For all Australians most of this spending is for chronic conditions like complications from diabetes, but, too often, Indigenous Australians are hospitalised for vaccine-preventable conditions like influenza and pneumonia, acute conditions like cellulitis, and injury.

Avoidable hospitalisations are an important indicator of effective and timely access to primary care, and provide a summary measure of health gains from primary care interventions. The inescapable reality is that current primary care interventions are not working.

We know what the problems are. Around two-thirds of the gap in health outcomes between Indigenous Australians and other Australians comes from chronic diseases such as cardiovascular disease, diabetes, respiratory diseases and kidney disease.4 Suicide and transport accidents and other injuries are also leading causes of death.5 Half of the gap in health between Indigenous and non-Indigenous Australians is linked to risk factors such as smoking, obesity and physical inactivity.6 A number of studies have found that between a third and half of the health gap is associated with differences in socioeconomic status such as education, employment and income.7

The 2006 Census (the latest available data) found that 39% of Indigenous people were living in “low resource” households (as defined by the Australian Bureau of Statistics8), almost five times the non-Indigenous rate.9 Such disparities in income limit Indigenous people’s capacity to pay for health care and provide some context for why they are more likely to use public hospitals than privately provided services that require copayments.

There are commitments from all the major stakeholders, political parties and policymakers to close the gap. There is a new National Aboriginal and Torres Strait Islander Health Plan 2013–2023. And, arguably, there are enough funds if these are spent wisely. What is needed is a new approach to how health care is developed for and delivered to Indigenous Australians.

The approach needs to be grounded in three broad principles:

  • Adhering to the principle of “nothing about me without me”.10 Shared decision making must become the norm, with patients and their needs at the centre of a system they drive.

  • Addressing the social determinants of health, in particular, the impact of poverty.

  • Addressing cultural barriers in the way that Indigenous people want.

These are not new ideas and all the right words are in the new national health plan, as they were in the previous strategy document — cross-portfolio efforts, partnership, sustainability, culturally competent services, community, a rights-based approach to providing equal opportunities for health. What we must do is move beyond these fine words to meaningful action.

We have the exemplar of how to do this with Aboriginal Community Controlled Health Organisations (ACCHOs), and we need to (i) provide increased opportunities for engagement, collaboration and service delivery with ACCHOs and (ii) expand this way of working into mainstream services. This will require a different approach to policy development and implementation.11

The key barriers to health care for urban and remote populations alike relate to availability, affordability and acceptability12 and the dominance of biomedical models of health.13 ACCHOs are a practical expression of self-determination in Indigenous health and health service delivery,14 and have been very successful at reducing many of the barriers that inhibit Indigenous access to mainstream primary care.15 Importantly, ACCHOs provide both cultural safety, which allows the patient to feel safe in health care interactions and be involved in changes to health services, and cultural competence, which reflects the capacity of the system to integrate culture into the delivery of health services.16

However, the success of the design and work practices of ACCHOs have had little influence on the mainstream health system17 which remains, necessarily, the source of health care for many Indigenous people. And it can be argued that the current funding and regulatory practices of Australian governments are a heavy burden and consume too much of the scarce resources of ACCHOs in acquiring, managing, reporting and acquitting funding contracts.18

Governments and all stakeholders, including Indigenous people themselves, need to be bold enough to redesign current mainstream health policies, programs and systems to better fit Indigenous health concepts, community needs and culture. This approach should not be seen as radical — it is where we are currently headed with Medicare Locals. We should not ignore the fact that ACCHOs have led the way in developing a model of primary health care services that is able to take account of the social issues and the underlying determinants of health alongside quality care.19 Tackling these reforms will therefore benefit all Australians, but especially those Indigenous people who currently feel disenfranchised. Without real and meaningful change, we are all condemned to more government reports bearing sad, bad news and a continual yawning gap of Indigenous disadvantage.

Training opportunities key to closing health gap

There are many factors contributing to the gap in health and life expectancy experienced by Aboriginal peoples and Torres Strait Islanders. These factors range from the adverse health impacts of early life circumstances, right through to the high prevalence of chronic cardiovascular diseases.

Research shows that chronic disease deaths could be halved among Aboriginal peoples and Torres Strait Islanders by timely and systematic diagnosis, and within a short period of time also. Similarly, appropriate culturally safe support from trained health and medical professionals for mothers and babies in the early years could ameliorate the life-long health impacts of a poor start in life for Aboriginal and Torres Strait Islander children.

A proper supply of health practitioners and medical professionals working with Aboriginal and Torres Strait Islander communities would go some way to breaking this circuit of poor health. However, what is most needed, but is in limited supply, are health and medical professionals who are fully skilled in best practice service provision to Aboriginal people and Torres Strait Islanders.

We know what best practice models of primary health care for Aboriginal people and Torres Strait Islanders involve (the AMA published a major report on this in 2011-12). But there are very few opportunities for doctors and health practitioners – either in training or once qualified – to gain hands on experience and excellence in skills and knowledge working in real situations with expert practitioners and researchers doing cutting edge work in Aboriginal health.

To rectify this the AMA believes that there is a great need for centres of excellence in Aboriginal and Torres Strait Islander health which can:

  • conduct research on models and approaches to health conditions and risks besetting Aboriginal people and Torres Strait Islanders;
  • provide best practice primary care services based on that research;
  • provide practical training and experience to doctors, health professionals and trainees who take visiting placements at the centres for varying periods of time; and
  • offer accreditation in Aboriginal and Torres Strait Islander health to those centres which take placements and meet requirements.

The AMA believes there needs to be a national network of these Teaching Health Centres of Excellence, given that different areas of Australia have different Aboriginal and Torres Strait Islander populations with different characteristics and needs.

To fulfil all the above roles, each Teaching Health Centre of Excellence would need to be formed as a collaboration between Aboriginal community-controlled health services, government health services and clinics, and universities involved in teaching and applied research in Aboriginal and Torres Strait Islander health.

Practical teaching would encompass students from medicine, nursing, allied health and Aboriginal Health Workers at Diploma, Advanced Diploma, Graduate and Post-Graduate level. As students and visiting doctors pass through these centres of excellence and take their posts up elsewhere, they could take back with them knowledge, skills and expertise in the delivery of high quality, culturally competent primary care.

The AMA has advocated for the establishment of a national network of Teaching Health Centres of Excellence in the past, and has resolved to impress upon the new Federal Government the need for these centres of innovation to close the gap.

Reform can fix health gap

Professor Ian Ring, Professorial Fellow at the Australian Health Services Research Institute, University of Wollongong, suggests the review of Indigenous funding being headed by Tony Mundine, Chair of the Federal Government’s Indigenous Advisory Council, could pave the way for real improvements in Aboriginal health.

This article was first published in The Canberra Times on 28 October, 2013.

A recent episode of Q&A echoed traces of the widespread view that much money has been spent on Aboriginal health and other matters, with relatively little to show for it – and that the money must have been eaten up by a bloated bureaucracy, was misdirected, or corruptly or incompetently used.

All of these may be true, but only to a very limited extent. The reality is that, until recently, the Federal Government, through its own programs, was spending less per capita on Aboriginal health than it was on the rest of the population – despite Aboriginal people being at least twice as sick.

That changed with the introduction of the National Partnership Agreements (NPAs) involving the Commonwealth and all State and Territory governments, which injected $1.6 billion into Aboriginal health and $4.6 billion over four years to 2012-13 into health, education, housing, employment and remote services as part of the Closing the Gap programs. Australia went from having a degree of international opprobrium because of its neglect of Aboriginal issues to becoming internationally competitive in terms of indigenous policy and funding.

But what results have we seen from this allocation of additional funds? In a four-year program, the funds start out at low levels in the first year and build up progressively over the next three. The funds then need to be used to employ people, who need to be recruited and trained, and then it takes more time for the programs in which they work to become fully effective.

Taking the $100 million allocated to smoking, for example, the very earliest we could hope to see any kind of significant change in smoking would be picked up by the next smoking surveys, the results of which will be available next year.

Given the lag between smoking reduction and improvements in smoking-related diseases, the earliest we could see measurable changes in heart and lung mortality may not be until 2020.

The apparent lack of progress from data currently available tells us about the lack of progress before the additional $1.6 billion hit the ground and is just what we would expect to see at this stage, rather than indicating a waste of funds or a misallocation of resources.

But was the money optimally allocated? Almost certainly not, and for reasons that are crying out to be dealt with by the Mundine review. The programs funded by the NPAs all made sense individually but, collectively, they missed the point, and in no sense approximated the comprehensive long-term action plan promised in the statement of intent. The problem was not in the policy determined by governments, or in the funding, but in the bureaucratic implementation of those policies.

The programs were determined by officials in State and Territory governments with insufficient genuine consultation with the people who run the Aboriginal community controlled health services (ACCHS).

Nobody seemed to have asked that, if we want to halve the child mortality gap in 10 years and the life expectancy gap in a generation, what services do we need to achieve those goals?

And nobody seems to have wondered how it was possible to have healthy mothers and babies, and to get on top of chronic diseases, without adequate provision for mental health services.

The limited evidence available clearly shows that ACCHS run by and for Aboriginal people eclipse mainstream general practice in the identification of risk factors, performance of health checks, care planning and the management of Aboriginal and Torres Strait Islander patients.

So, instead of asking what services would produce the best return on investment, the decision seems to have been taken to allocate new funds to perpetuate current patterns of use between mainstream and ACCHS health services.

Too many senior officials still cling to the notion that in Australia’s cities and towns mainstream services are the answer – in the absence of evidence that this is so, and in the face of evidence that it isn’t. There is a real risk that mainstreaming will be seen as some kind of solution, when the reality is that there needs to be sensible arrangements for mainstream and ACCHS services to work together, as in the Urban Indigenous Health Institute.

While current levels of indigenous health funding go a long way to redressing the previous shortfall in health expenditure, estimated by health economists at about $500 million a year, inequities in the share of mainstream program funding received by Aboriginal people is still an issue.

So what does this mean for the Mundine review and the new Government? Three issues stand out.

First, bureaucratic reform is essential. That means substantially fewer public servants, but those that remain need to have the requisite skills and experience. There is broad agreement that the main functions of Aboriginal health should remain with the Department of Health, preferably led by an Indigenous official. But a small, high-level group in the Department of the Prime Minister and Cabinet, to ensure that the new Prime Minister’s requirement to deliver for Aboriginal people is met, is an essential component of the new arrangements.

Second, the recently formulated National Aboriginal and Torres Strait Islander Health Plan isn’t really a plan in any meaningful sense, but could become one if the implementation plan foreshadowed in it is developed in genuine partnership with Aboriginal people, and involves officials with the requisite skills, experience and training. But that implementation plan needs to also include mental health and, this time, to wrestle successfully with mainstreaming.

Third, and most important, it is time for Aboriginal communities to play a more central role in the design and conduct of their own services, bearing in mind that some of the best health services in Australia are run by the ACCHS sector.

If the Mundine review and the Abbott government can successfully address these issues Australia, in the not too distant future, could complete the long transition from international opprobrium to leading the world in Indigenous health.

Utility of exercise electrocardiography testing for the diagnosis of coronary artery disease in a remote Australian setting

Coronary artery disease (CAD) remains the leading cause of death in Australia, both in the general population and also among Aboriginal and Torres Strait Islander peoples (referred to henceforth as Indigenous Australians).1 Indigenous Australians are three times as likely to suffer a major coronary event than are non-Indigenous Australians,2 and cardiovascular disease remains the leading cause of Indigenous mortality and the main contributor to the mortality gap between Indigenous and non-Indigenous Australians.3 Furthermore, the burden and severity of other diseases that predispose to CAD are higher among Indigenous Australians.4

Patients with an acute coronary syndrome (ACS), as defined by electrocardiography results and biochemical markers, proceed to coronary angiography, which is considered the gold standard diagnostic tool for CAD; however, its use is limited due to its invasive nature, cost and accessibility.5 In the absence of a definite ACS, less invasive, and often more accessible, exercise stress testing is used. Stress testing determines the significance of a patient’s symptoms by indicating whether functional myocardial ischaemia occurs and therefore whether further investigations, including coronary angiography, are needed.

Alice Springs Hospital (ASH), in the Northern Territory, services a dispersed population of 45 000 people spread over 1 million square kilometres, of whom 44% are Indigenous Australians.6 ASH is about 1500 kilometres from the nearest angiography facilities and relies on exercise electrocardiography testing (EET) to prioritise patients for further investigation of possible CAD. Patients with a “positive” test are typically referred for coronary angiography, and patients with a “negative” test are usually reassured and assumed to be at low risk of significant CAD.7 Inconclusive test results typically lead to referral for stress echocardiography — the timing of which is reliant on the frequency of visiting cardiologists. Consequently, the results of EET are heavily relied upon to inform a diagnosis and management plan. In non-Indigenous populations, the usefulness of EET has been reflected in its reported high negative predictive value of 99%.8–11 We chose to retrospectively audit the performance of EET in our local population, as its diagnostic utility in a setting with a significant proportion of Indigenous Australians has not been studied. In addition, we assessed the significance of inconclusive EET results with regard to subsequent clinical outcomes, as patients with inconclusive results may be at increased risk of CAD-related events while waiting for further diagnostic testing.

Methods

We undertook a retrospective audit of data for patients with suspected CAD who underwent EET between 1 June 2009 and 31 May 2010. We excluded patients with a pre-existing diagnosis of CAD and those not permanently residing in the NT. Data collected included patient demographics, CAD risk factors, results of the EET, and clinical outcomes for the following 2 years as documented in the patients’ medical records.

ASH uses the Bruce protocol for conducting EET, aiming to achieve a target age- and sex-based heart rate, exercise duration and workload (based on metabolic equivalents [METS]).9 A positive result was one or more of: angina during exercise; ST-segment depression that was > 1 mm and/or downsloping; reduction in blood pressure of > 10 mmHg from baseline and/or multiple ventricular premature complexes or runs of ventricular tachycardia. A negative test result was recorded if the patient was asymptomatic with a normal electrocardiogram and blood pressure response on completion of maximal testing. A patient who failed to complete the test for reasons other than those that would classify the test as being positive was reported as having an inconclusive test result.10

Clinical outcomes were reviewed for 2 years after EET for details of subsequent coronary angiography results consistent with CAD, readmission to ASH for investigation of chest pain and readmission to ASH with a separation diagnosis of an ACS. Our assessment of the overall utility of EET was based on the risk of having a coronary angiogram suggestive of either CAD or an ACS within 24 months of testing.

Statistical analysis was undertaken using Stata12 (StataCorp). Continuous variables were compared using the Wilcoxon rank-sum test; categorical variables were compared using the χ2 test. Continuous non-parametric data are presented as medians with interquartile range, and categorical variables are presented as percentages with binomial confidence intervals. Logistic regression models were created using a backwards stepwise approach, including in the first model all variables shown in univariable models to be related to test outcome, as well as variables that differed between Indigenous and non-Indigenous subjects at baseline. All statistical tests were two-sided and P less than 0.05 was taken to indicate statistical significance. Ethics approval for the study was provided by the Central Australian Human Research Ethics Committee.

Results

We reviewed the medical records and EET results of 268 patients who met our inclusion criteria. Descriptive data related to these patients are presented in Box 1. Indigenous identity was not reported for 10/268 patients (3.7%). Indigenous patients were significantly younger than non-Indigenous patients and were more likely to be women. They were also twice as likely to have been diagnosed with one or more chronic diseases (OR, 2.0; 95% CI, 1.1–3.7), particularly diabetes mellitus (OR, 5.9; 95% CI, 3.3–10.7) and chronic kidney disease (OR, 12.2; 95% CI, 4.1–36.1), compared with non-Indigenous patients.

The results of EET and outcomes over the subsequent 24 months are outlined in Box 2. Indigenous patients were less likely to reach a maximum heart rate or adequate workload (> 10 METS) (OR, 10.3; 95% CI, 5.3–20.3). In turn, this translated to a higher proportion of Indigenous patients having inconclusive test results compared with non-Indigenous patients (57/108 v 32/150; P < 0.001) and a lower proportion having positive (6/108 v 21/150; P = 0.03) and negative (45/108 v 97/150; P < 0.001) test results (Box 2). In logistic regression modelling, the major factors independently associated with an inconclusive result were a diagnosis of one or more chronic diseases (OR, 6.0; 95% CI, 2.5–14.1) and identifying as Indigenous (OR, 3.7; 95% CI, 2.1–6.6).

Compared with patients with an inconclusive or negative EET result, patients with a positive result were more likely to proceed to coronary angiography (21/34; P < 0.001) and were significantly more likely to present to hospital with chest pain in the following 2 years (11/28; P = 0.001). Indigenous patients were less likely than non-Indigenous patients to proceed to coronary angiography (10/34 v 24/34, respectively; P = 0.114), and more likely to present with an ACS in the following 2 years (4/108 v 2/139, respectively; P = 0.25); however, neither of these differences were statistically significant. Overall, the risk of presenting with an ACS within 24 months significantly increased as the result of EET moved from negative to inconclusive to positive (OR, 4.4; 95% CI, 1.4–14.0). A similar relationship to EET results was seen for re-presentation with chest pain within 12 months (OR, 2.0; 95% CI, 1.3–3.1) and re-presentation with chest pain within 24 months (OR, 2.0; 95% CI, 1.3–2.9).

The sensitivity, specificity and positive and negative predictive values of EET in our sample are summarised in Box 3.

Discussion

EET clearly represents a cheap, non-invasive diagnostic modality for screening patients presenting with suspected CAD. Our findings provide reassurance that, when maximal testing can be completed, EET has performance characteristics that are at least equivalent to those reported in the literature.8 Even when inconclusive results were included, the lack of a positive EET continued to confer a low risk of a subsequent presentation with an ACS. While the presence of chronic disease was the main predictor of an inconclusive EET there was also an independently elevated risk associated with being Indigenous. This may be related to physical and social factors, including familiarity with treadmill exercise, and fitness.

A focus should be to reduce the proportion of inconclusive tests. In general, an image-based myocardial stress study, typically echocardiography with dobutamine, is performed when the EET result is inconclusive. These tests are conducted by visiting cardiologists, but waiting periods are variable and may extend to months. In the interim, a person with possible CAD may go without treatment and be at risk of a preventable adverse outcome — demonstrated in our study by the high rates of loss to follow-up and re-presentation with an ACS. Possible solutions include enhanced orientation and education of patients before they undergo EET, and greater use of Indigenous language translators.

Our study was limited by its reliance on retrospective collection of data that were non-standardised. The information gathered was limited to data documented at the time of the EET. Similarly, follow-up of patients re-presenting with ACS or chest pain was restricted to those who presented to ASH. Nonetheless, as the only referral hospital servicing the Central Australian region, most clinically significant events in remote clinics would have been captured. This limitation could be overcome by repeating the audit prospectively.

In summary, EET is likely to remain a useful and important tool in determining the risk of CAD among patients in regional and remote Australian locations where onsite specialist cardiology services are limited. Further attention should be given to how inconclusive test results could be reduced. Positive initiatives may include greater involvement of Indigenous people in the health care workforce associated with EET, exploring patients’ understanding of the concepts of CAD and exercise, and educating patients and health care providers. Greater use of myocardial stress testing modalities that do not require specialist cardiologists, such as cardiac computed tomography angiography, or training local staff to perform stress echocardiography could also be considered as means of enhancing the care of patients with inconclusive results.

1 Descriptive details of 268 patients who underwent exercise electrocardiography testing 1 June 2009 – 31 May 2010

All patients

Indigenous patients

Non-Indigenous patients

No.

Proportion (95% CI)*

No.

Proportion (95% CI)*

No.

Proportion (95% CI)*

P†

Age in years, median (IQR)

–

49.0 (41.6–57.5)

–

45.7 (39.1–55.3)

–

51.0 (44.9–58.6)

0.004‡

Total number

268

100%

108

40.3%

150

56.0%

–

Women

118

44.0% (38.0%–50.2%)

64

59.3% (50.0%–68.7%)

52

34.7% (27.0%–42.4%)

< 0.001

History of smoking

103/245

42.0% (35.8%–48.5%)

48/100

48.0% (37.9%–58.2%)

55/145

37.9% (30.0%–46.4%)

0.12

Family history of CAD

67/155

43.2% (35.3%–51.4%)

24/45

53.3% (37.9%–68.3%)

43/110

39.1% (29.9%–48.9%)

0.10

Any chronic disease

189/262

72.1% (66.3%–77.5%)

88/108

81.5% (72.9%–88.3%)

101/148

68.2% (60.1%–75.6%)

0.02

Diabetes mellitus

80/250

32.0% (26.3%–38.2%)

57/107

53.3% (43.7%–62.9%)

23/143

16.1% (10.0%–22.2%)

< 0.001

Hypertension

132/252

52.4% (46.0%–58.7%)

71/107

66.4% (56.6%–75.2%)

61/145

42.1% (33.9%–50.5%)

< 0.001

Dyslipidaemia

139/237

58.6% (52.1%–65.0%)

71/98

72.4% (62.5%–81.0%)

68/139

48.9% (40.4%–57.5%)

< 0.001

Renal impairment (eGFR < 60 mL/min/1.73 m2)

18/215

8.4% (5.0%–12.9%)

14/98

14.3% (8.0%–22.8%)

4/111

3.6% (1.0%–9.0%)

0.02

Albuminuria (ACR > 3.4 mg/mmol)

26/48

54.2% (39.2%–68.6%)

25/38

65.8% (48.6%–80.4%)

1/8

12.5% (0.3%–52.7%)

0.02

Renal impairment or albuminuria

35/216

16.2% (11.6%–21.8%)

31/99

31.3% (22.4%–41.4%)

4/111

3.6% (1.0%–9.0%)

< 0.001

* Unless otherwise indicated. † χ2 unless otherwise indicated. ‡ Wilcoxon rank-sum test. ACR = albumin : creatinine ratio. CAD = coronary artery disease.
eGFR = estimated glomerular filtration rate. IQR = interquartile range.

2 Exercise electrocardiography testing results and patient outcomes

All patients

Indigenous patients

Non-Indigenous patients

No.

Proportion (95% CI)*

No.

Proportion (95% CI)*

No.

Proportion (95% CI)*

P

Exercise electrocardiography test result

Positive

31/268

11.6% (8.0%–16.0%)

6/108

5.6% (2.1%–11.7%)

21/150

14.0% (8.9%–20.6%)

0.03

Inconclusive

90/268

33.6% (28.0%–39.6%)

57/108

52.8% (42.9%–62.5%)

32/150

21.3% (15.1%–28.8%)

< 0.001

Negative

147/268

54.9% (48.7%–60.9%)

45/108

41.7% (32.3%–51.5%)

97/150

64.7% (56.5%–72.3%)

< 0.001

Coronary angiography performed

34/268

12.7% (8.9%–17.3%)

10/108

9.3% (4.5%–16.4%)

24/150

16.0% (10.5%–22.9%)

0.11

Proportion of coronary angiograms that were positive

18/34

52.9% (35.1%–70.2%)

5/10

50.0% (18.7%–81.3%)

13/24

54.2% (32.8%–74.4%)

0.82

Acute coronary syndrome

Within 1 year

4/263

1.5% (0.4%–3.8%)

3/108

2.8% (0.6%–7.9%)

1/145

0.7% (0–3.8%)

0.12

Within 2 years

6/255

2.4% (0.9%–5.1%)

4/108

3.7% (1.0%–9.2%)

2/139

1.4% (0.2%–5.1%)

0.25

Acute coronary syndrome and/or positive angiogram

Within 1 year

20/263

7.6% (4.7%–11.5%)

7/108

6.5% (2.6%–12.9%)

13/145

9.0% (4.9%–14.8%)

0.47

Within 2 years

21/255

8.2% (5.2%–12.3%)

8/108

7.4% (3.3%–14.1%)

13/139

9.4% (5.1%–15.5%)

0.59

Readmission with chest pain

Within 1 year

55/264

20.8% (16.1%–26.2%)

28/108

25.9% (18.0%–35.2%)

25/146

17.1% (11.4%–24.2%)

0.09

Within 2 years

67/256

26.2% (20.9%–32.0%)

35/108

32.4% (23.7%–42.1%)

30/140

21.4% (14.9%–29.2%)

0.05

* Unless otherwise indicated.

3 Diagnostic utility of exercise electrocardiography testing*

Prevalence of outcome†

Sensitivity

Specificity

Positive predictive value

Negative predictive value

All patients

All test results (n = 268)

8.5% (5.2%–12.3%)

61.9% (38.4%–81.9%)

94.0% (90.2%–96.7%)

48.1% (28.7%–68.1%)

96.5% (93.2%–98.5%)

Inconclusive results excluded (n = 178)

9.0% (5.1%–14.4%)

86.7% (59.5%–98.3%)

90.8% (85.0%–94.9%)

48.1% (28.7%–68.1%)

98.6% (94.9%–99.8%)

Indigenous patients

All test results (n = 108)

7.4% (3.3%–14.1%)

37.5% (8.5%–75.5%)

97.0% (91.5%–99.4%)

50.0% (11.8%–88.2%)

95.1% (88.9%–98.4%)

Inconclusive results excluded (n = 51)

9.8% (3.3%–21.4%)

60.0% (14.7%–94.7%)

93.5% (82.1%–98.6%)

50.0% (11.8%–88.2%)

95.6% (84.9%–99.5%)

Non-Indigenous patients

All test results (n = 150)

9.4% (5.1%–15.5%)

76.9% (46.2%–95%)

93.7% (87.9%–97.2%)

55.6% (30.8%–78.5%)

97.5% (92.9%–99.5%)

Inconclusive results excluded (n = 118)

9.2% (4.5%–16.2%)

100% (69.2%–100%)

91.9% (84.7%–96.4%)

55.6% (30.8%–78.5%)

100% (96.0%–100%)

* All values are % (95% CI). † Defined as coronary angiogram suggestive of coronary heart disease or an acute coronary syndrome within 24 months of testing.

Cooperation vital to close health gap

The AMA has urged the Federal, State and Territory government to put partisanship to one side and begin to work together on plans to boost Aboriginal and Torres Strait Islander health.

AMA President Dr Steve Hambleton welcomed the long-awaited launch last week of the Commonwealth’s National Aboriginal and Torres Strait Islander Health Plan as an important first step in developing a coordinated approach to dramatically improve Indigenous health in the next 10 years.

The Plan, developed in partnership with Aboriginal and Torres Strait Islander people, calls for a greater focus on child health and development and the social determinants of illness and disease as part of efforts to close the gap and establish health equality by 2031.

Indigenous Health Minister Warren Snowdon said that the Government was determined, with the support of peak Indigenous groups including the National Aboriginal Community Controlled Health Organisation, to take a broader approach to Indigenous health to encompass developmental and social issues including violence and alcohol abuse as well as stamping out racism and inequality in the health system.

“In this plan we signal the need to expand our focus on children’s health to broader issues in child development,” Mr Snowdon said. “We have much more work to do in developing robust research and data systems. I am also resolved that we will tackle the difficult and distressing issues of violence, abuse and self harm.”

Shadow Indigenous Health Minister Andrew Laming said the Plan was an essentially empty statement short on detail, and accused the Government of springing the announcement on Indigenous health groups.

“The plan…contains little detail,” Dr Laming told The Australian. “[It] appears to be yet another exercise in political spin, lacking any substance, and fails to say how we are going to get there.”

But Mr Snowdon said the plan, developed following a series of 17 consultations held with Aboriginal and Torres Strait Islander communities and the receipt of more than 140 written submissions, would provide guidance for State and Territory governments about what the Commonwealth saw as priorities, and make sure they were taken into account in future intergovernmental agreements to improve Indigenous health.

The Minister used the announcement to intensify the pressure on the states and territories yet to commit to a new five-year National Partnership Agreement on Closing the Gap in Indigenous Health Outcomes after the first deal expired last month.

So far, only the Commonwealth and Victoria have committed to a new five-year agreement, while Western Australia has pledged funds for just one year.

Dr Hambleton said a renewed agreement was vital, not only to ensure recent improvements in Indigenous health were sustained and built upon, but also to shepherd through the changes outlined in the Federal Government’s Health Plan.

The AMA President said that, now the Plan had been released, there needed to be detailed and comprehensive commitments from all those involved  – governments and medical and community groups – to ensure it was implemented.

Dr Hambleton said clear and measurable targets should be developed, as well as plans for how they were to be met.

He said this needed to be underpinned by appropriate funding and strategies to ensure the necessary workforce was available.

Underlying it all, he said, there had to be a solid requirement that all governments work together in genuine partnership, and with the guidance of Indigenous health leaders and communities.

“A National Implementation Plan is not truly national unless it has all the states and territories on board in a spirit of cooperation with the Commonwealth,” the AMA President said.

Adrian Rollins

 

Birthweight and fasting glucose and insulin levels: results from the Aboriginal Birth Cohort Study

The concerning rise in type 2 diabetes in Indigenous populations continues, with different hypotheses put forward to explain the phenomenon. International evidence links the fetal nutrition proxies of low birthweight (LBW) and fetal growth restriction (FGR) to chronic diseases in adult life.1 The developmental origins of health and disease (DOHaD) hypothesis states that undernutrition in utero results in permanent changes through epigenetic mechanisms that later influence disease development (http://www.mrc. soton.ac.uk/dohad). The highest risk for type 2 diabetes is reported when LBW or FGR is followed by later overweight or obesity, suggesting a mismatch between intrauterine and postnatal nutrition.2

Despite recent improvements, Australian Aboriginal LBW rates remain double those of the non-Aboriginal population.3 National Aboriginal rates of FGR are unknown, but in a Northern Territory study, 25% of Aboriginal newborns were defined as fetal growth restricted.4

Concurrently, not only are Australian Indigenous rates of overweight and obesity increasing — they currently range from 37% for ages 15–24 years to 74% for those aged over 55 years5 — but 10%–30% of Aboriginal people are now estimated to have type 2 diabetes.6

The high-risk combination of LBW and later obesity has been shown to be the greatest risk for elevated blood pressure in a cross-sectional community study of a NT Aboriginal population.7 More recently, a retrospective study in one NT community linked LBW and later chronic disease in Australian Aboriginal people8 and suggested LBW may be a contributor to the current high rates of type 2 diabetes in the Aboriginal population.

Using data from a prospective life-course Aboriginal birth cohort study, our aim was to examine the relationships of glucose and insulin metabolism with birth and current adolescent size.

Methods

We conducted a prospective life-course study of an NT Aboriginal birth cohort.

The recruitment and follow-up of this birth cohort has been previously published.9,10 In brief, 686 Aboriginal babies out of a possible 1238 born at the Royal Darwin Hospital (1987–1990) were recruited into the study. There were no significant differences in the mean birthweight, sex ratio or birthweight frequencies between those recruited (686), those with gestational age estimation (603) and those not recruited. At follow-up (2005–2008) in over 40 NT locations, 68 participants could not be found (9.9%). Of the remainder, 27 had died, 11 refused consent, 111 were traced but were unable to be examined for logistical reasons,10 and 469 who had complete perinatal and adolescent data were examined.

The birth measures of weight, gestational age estimations and follow-up anthropometric measures have previously been described.4,10 Within 4 days of birth, the same neonatal paediatrician performed a gestational age assessment using the Dubowitz scoring system.11 LBW was defined as birthweight < 2500 g, FGR as birthweight < 10th percentile for gestational age, and large for gestational age as birthweight > 90th percentile for gestational age, using an Australian population reference standard contemporary with cohort recruitment.12

Adolescents were measured in light clothing while barefoot. Height was measured to the nearest millimetre using a portable stadiometer and weight was measured to the last complete 0.1 kg with a digital electronic scale (TBF-521, Tanita).

Participants were asked to fast from midnight before the examination. Blood samples were taken at the time of examination, collected in fluoride oxalate tubes after application of anaesthetic cream to the venepuncture site, separated after collection (for a minority of samples, this was up to a maximum of 2–3 hours) and transported in cold-boxes to Darwin.

Fasting glucose levels were measured enzymatically using a modular analyser (Roche Diagnostics), fasting insulin levels were measured by immunoassay (AxSYM, Abbott Laboratories), and glycated haemoglobin concentrations by high-pressure liquid chromatography (PDQ, Primus Diagnostics). Insulin resistance was estimated from fasting insulin and glucose concentrations using homoeostatic model assessment (HOMA-IR).13

Cross-sectional growth outcomes were described by z scores for weight for age (WAZ) and height for age (HAZ) using the 2000 Centers for Disease Control and Prevention (CDC) sex-specific growth reference.14 Undernutrition was defined as 2 standard deviations (SDs) below zero and overweight was defined as 2 SDs above zero, according to World Health Organization criteria.15

Fasting was defined as an overnight fast of 8 hours or more, and 134 participants satisfied this criterion and had complete perinatal and follow-up data.

Residence at the time of follow-up was defined as remote (residence in defined remote Aboriginal communities) or other (including the twin cities of Darwin and Palmerston and the greater Darwin area).

Statistical analysis

The clinical characteristics were summarised as means (SD), and if not normally distributed, as geometric means (SD) and as category percentages. Characteristics were compared between sexes using the t test (for normally distributed values) and the χ2 test (for categorical values). Non-normal data were transformed to yield normal distribution before t tests were performed.

Representativeness of the fasting sample, as described above, was tested using t, Wilcoxon and χ2 tests, depending on the distribution of the test variable.

For analyses, birthweight, and adolescent height, weight and body mass index (BMI) were continuous variables, while birthweight for gestational age was dichotomised at the 10th percentile for FGR and at the 90th percentile for large for gestational age.

The relationships of fasting insulin, glucose and HOMA-IR measures to the birth size and current adolescent size were each analysed in standard regression models using the approach recommended by Lucas and colleagues16 adjusted for gestational age, sex, and contemporary age using Stata, version 11 (StataCorp).

In order to maintain the assumptions of regression-dependent variables, fasting insulin, glucose and HOMA-IR values were transformed using the natural log transformation. Each outcome variable was tested in separate univariate models for each of the birth measures (eg, model 1), then adjustment for height (eg, model 1a) or weight (eg, model 1b) was added to the model, then an interaction term between the birth measures and adolescent weight or height was added. Lastly, the outcome variables were tested in separate univariate models for adolescent height (eg, model 3) and weight (eg, model 4). Models were separately analysed with current-residence regression coefficients and were then back-transformed using exponentiation, presenting ratios for ease of interpretation.

The percentage of total variance in the outcome measures, accounted for by early life size and later adolescent size, were estimated by the difference in the coefficients of determination (R2) between fully adjusted birth models with and without the measure of interest.

Ethics

The Human Research Ethics Committee of the Northern Territory Department of Health and Families and Menzies School of Health Research, including the Aboriginal Ethics Sub Committee, which has the power of veto, approved the study. Written consent was obtained in the form of an itemised consent with participants allowed to refuse individual procedures.

Results

One hundred and thirty-four participants had complete perinatal and follow-up data and fasting insulin and glucose measures. Box 1 shows the comparison of the fasting subset with the complete cohort and the subset of participants who did not have fasting values. This fasting subset was not significantly different from the non-fasting subset in the perinatal measures, the follow-up measures and the levels of non-fasting biomarkers (glycated haemoglobin and C-reactive protein) associated with type 2 diabetes. There were 59 males and 75 females with a mean age of 18.14 (SD, 1.1) years. The birth and adolescent characteristics of this fasting subset are shown in Box 2. As expected, females were significantly shorter (P < 0.01) and lighter (P < 0.01). Only one participant had a fasting glucose > 7 mmol/L and there were no participants with fasting glucose values of 6.1–6.9 mmol/L.

For the fasting dataset, using the international CDC reference,14 the mean WAZ scores were negative for both males and females. The proportions of males and females with WAZ < − 2 (undernutrition) were 18.6% and 17.3%, respectively. At follow-up, none of the 33 fasting adolescents who had been fetal growth restricted at birth had a WAZ > 2 (overweight/obesity). Only one participant had a WAZ > 1, with a similar profile occurring for those who had LBW.

Birthweight had a significant positively directed association with fasting glucose but not with fasting insulin levels. For every kg increment in birthweight, adolescent fasting glucose levels rose by 7% (P = 0.002) (Box 3). This positively directed association of birthweight with fasting glucose levels remained after adjustment for adolescent height or weight, which accounted for 6% and 3% of the variation in fasting glucose levels, respectively.

The significant association with fasting glucose levels also remained when birthweight was categorised as birthweight for gestational age. For adolescents who had been fetal growth restricted at birth, fasting glucose levels were 7% less than for those who were not fetal growth restricted at birth (P = 0.003), and these relationships remained the same after adjustment for adolescent height and weight, again accounting for 6% and 3% of the variation in fasting glucose levels (Box 3).

Current height, weight and BMI had significant and positively directed associations with both fasting insulin and glucose levels in univariate models, with the regression ratio and percentage of variation explained being greatest for the fasting adolescent insulin and HOMA-IR measures.

For every kg increment in weight, cm increment in height or index point in BMI, fasting insulin levels rose by 3%, 3% and 9%, respectively (Box 4), and HOMA-IR by 3% (95% CI, 1.02–1.04; P < 0.01), 3% (95% CI, 1.01–1.06; P = 0.01) and 10% (95% CI, 1.08–1.13), respectively (data for HOMA-IR not shown), while for fasting glucose, the changes were 0.1% increase for every kg increment in weight, 0.2% for every cm increment in height, and 0.7% for every index point in BMI (Box 3).

Repeat analysis of all models with the inclusion of the remote status variable did not change any of the associations previously found. Regression models (models 3, 4 and 5 in Box 3 and Box 4) of height, weight and BMI were also reanalysed, with adjustment for birthweight, which did not change the results presented.

Apart from these main effects, there were positive and significant interactions between birthweight and height for insulin (P = 0.006) and HOMA-IR (P = 0.015) (data not shown). This allows for an extra increment in insulin and HOMA-IR values for participants who moved from higher birthweight to higher adolescent height. Hence, for a fixed current height, those adolescents with higher birthweights had higher measures of insulin and HOMA-IR values.

Discussion

In this adolescent cohort, there were no negatively directed associations between birthweight and either fasting glucose, insulin concentrations or the insulin-resistance measure, with no evidence of the U-shaped associations described for populations with similar high rates of type 2 diabetes in adult life. A positively directed association occurred for birthweight with fasting glucose levels. Consistent with these findings, those adolescents who had been fetal growth restricted at birth had lower fasting glucose concentrations. In contrast, even in this young and lean population, there were positively directed associations of current adolescent height and weight with fasting glucose and insulin concentrations and the insulin-resistance measure, albeit of a relatively trivial magnitude for fasting glucose. For fasting glucose levels, the effect of birthweight and current weight was similar (R2, 0.070 v 0.076), but for fasting insulin levels, the effect of current weight was considerably stronger than birthweight (R2, 0.299 v 0.019). These overall findings are similar to findings for these Aboriginal cohort participants at 11 years of age.17

The proportions of males and females with undernutrition (WAZ < − 2) were 18.6% and 17.3%, respectively, which far exceeded the expected 2.3% using the CDC sex-specific growth reference.14 Hence, compared with this international reference, there was a marked excess of undernutrition in this cohort. Importantly, the findings of no associations between LBW and FGR with higher fasting adolescent insulin and glucose levels were contrary to the DOHaD hypothesis, and suggest that the adverse effects of poor fetal nutrition may be concealed by the persistent undernutrition in these Aboriginal adolescents.

The main strength of this study is that the data have been prospectively collected from a contemporary Australian Indigenous population. This is in contrast to many of the other studies examining the DOHaD hypothesis, which are retrospective studies.

Unusually for this type of cohort, at the time of recruitment less than 10% of mothers had homebirths.9 The single-point tertiary hospital recruitment meant birth measurements were standardised, and reliable gestational age estimations were all made by the one neonatal paediatrician within 4 days of birth. Hence, the better fetal growth surrogate of birthweight adjusted for gestational age was available for analysis. Further, all follow-up biological measures were directly collected.

The difficulty in obtaining reliable fasting blood samples in the field is reflected in the small sample size. However, a number of significant associations were present despite this sample size. A further limitation due to the age of participants is the necessity of using intermediary biomarkers of diabetes instead of the preferred specific disease end point. Socioeconomic status (SES) factors are potential confounders in this study and standard SES indicators were collected, such as years of schooling, house ownership and employment. There are limitations of standard measures in capturing the multidimensional differences within populations similar to this cohort population.18 In the absence of adequate discriminatory measures of SES, we used only remote current residence as an objective surrogate measure of SES. Including this variable made only a limited difference to the significance of one association.

Our findings are in contrast to the predominant literature of the DOHaD hypothesis describing inverse associations between birthweight and later fasting insulin and glucose levels. While these reports are mainly retrospective studies from developed populations,1 similar findings have been reported from Aboriginal populations19 and five low- or middle-income-country birth cohorts.20

Similar findings to our study have been reported in a young lean population of Guatemalan men and women at a mean age of 24 years.21 Further, in the Newcastle Thousand Families Study, at 49–51 years of age, adult lifestyle factors explained larger proportions of variances for fasting and 2-hour glucose compared with early-life measures.22,23 A contemporary study of British children, based on maternal recall of birthweight, reports current size as the main determinant of insulin and glucose concentrations in childhood.24

The growth outcomes in our study suggest that a major nutritional mismatch between fetal and adolescent life has not occurred. It is likely that the permanent changes in response to undernutrition in utero have remained appropriate in this undernourished adolescent population with low rates of the high-risk combination of LBW- or FGR-associated later obesity or overweight.

Given the high prevalence of overweight and obesity currently seen in the adult Aboriginal population,6 it is likely that the growth trajectory will positively change in this cohort and the high-risk combination for chronic disease of LBW or FGR followed by overweight or obesity will become more common over the next decade. Then the relationships of LBW or FGR with chronic biomarkers may become apparent, consistent with the DOHaD hypothesis. With the follow-up of this cohort at the age of 26 years currently underway, we are well placed to determine if and when the effects of poor intrauterine nutrition are potentiated by the onset of overweight and obesity.

In the meantime, our findings suggest that the current high rates of type 2 diabetes observed in the adult Aboriginal population are more likely to be decreased by strategies targeted to improve lifestyle factors in childhood and adolescence, rather than those focusing on improving birthweight alone.

1 Comparison of the fasting sample and the original cohort: Aboriginal Birth Cohort 1987–2008

Mean (SD)*

Characteristic

Original cohort with
gestational age data
(n = 603)

Fasting participants
with complete data
(n = 134)

P†

Birthweight, g

3013 (654)

3027 (689)

0.78

Low birthweight‡

18.2%

16.4%

0.54§

Gestational age, weeks

38.74 (1.96)

38.67 (2.11)

0.69

Fetal growth restriction**

27.5%

24.6%

0.39§

Large for gestational age††

7.8%

9.7%

0.35§

Male

52.9%

44.0%

0.28§

Remaining original cohort at follow-up
(n = 469)

Current age, years

18.30 (1.09)

18.14 (1.12)

0.06

Weight for age, z score

− 0.63 (1.62)

− 0.47 (1.63)

0.20

Height for age, z score

− 0.28 (0.92)

− 0.21 (0.97)

026

Body mass index, kg/m2

21.49 (5.63)

21.68 (5.47)

0.63

Glycated haemoglobin

5.20% (0.40%)

5.18% (0.42%)

0.49

C-reactive protein, mg/L

5.02 (7.48)

4.99 (7.78)

0.97

SD = standard deviation. * Unless otherwise specified. † t test unless otherwise specified. ‡ < 2500 g. § χ2 test. Wilcoxon test. ** Birthweight < 10th percentile for gestational age. †† Birthweight > 90th percentile for gestational age.

2 Birth and current adolescent characteristics of 134 fasting Aboriginal adolescents

Mean (SD)*

Characteristic

Total (n = 134)

Male (n = 59)

Female (n = 75)

P†

Perinatal

Birthweight, g

3027 (689)

3178 (730)

2908 (635)

0.02

Gestational age, weeks

38.7 (2.1)

38.7 (2.4)

38.6 (1.9)

0.79‡

Low birthweight§

16.4%

10.2%

21.3%

0.08

Fetal growth restriction

24.6%

20.3%

28.0%

0.31

Large for gestational age**

9.7%

11.9%

8.0

0.56

Adolescent

Age, years

18.14 (1.12)

18.11 (1.01)

18.17 (1.20)

0.77

Weight, kg

61.49 (20.06)

70.37 (23.74)

54.5 (13.0)

< 0.01‡

Weight for age, z score

− 0.47 (1.62)

− 0.24 (1.74)

− 0.65 (1.52)

0.15

Weight for age, z score < − 21

17.9%

18.6%

17.3%

0.84

Height, cm

167.33 (9.26)

174.41 (7.61)

161.76 (6.12)

< 0.01

Height for age, z score

− 0.21 (0.97)

− 0.21 (1.02)

− 0.21 (0.95)

0.98

Height for age, z score − 214

3.0%

5.1%

1.3%

0.32††

Body mass index, kg/m2

21.68 (5.47)

22.83 (6.35)

20.78 (4.50)

0.04‡

Weight for age, z score > 215

6.7%

13.5%

1.3%

0.09

Fasting glucose, mmol/L

4.64 (0.59)

4.78 (0.46)

4.53 (0.65)

0.01‡

Fasting insulin, mU/L

8.36‡‡ (2.40)

7.47‡‡ (2.54)

9.16‡‡ (2.28)

0.19

HOMA-IR

1.71‡‡ (2.53)

1.58‡‡ (2.71)

1.83‡‡ (2.39)

0.38

Glycated haemoglobin

5.16%‡‡ (1.08%)

5.19%‡‡ (1.08%)

5.14%‡‡ (1.08%)

0.48

C-reactive protein, mg/L

1.88‡‡ (4.84)

2.03‡‡ (4.07)

1.78‡‡ (5.53)

0.64

HOMA-IR = insulin resistance estimated using homoeostatic model assessment. SD = standard deviation. * Unless otherwise specified. † t test unless otherwise specified. ‡ Unequal t test. § < 2500 g. Birthweight < 10th percentile for gestational age. ** Birthweight > 90th percentile for gestational age. †† Fisher’s exact test. ‡‡ Geometric mean.

3 Size at birth and adolescent height and weight: relationships with fasting glucose (mmol/L) concentrations among Aboriginal adolescents (n = 134)*

Model

Ratio

95% CI

P

R2†

Model 1: birthweight, kg

1.07

1.03–1.11

0.002

0.070

Model 1a: adjusted for child height

1.07

1.02–1.11

0.005

0.057

Model 1b: adjusted for child weight

1.05

1.00–1.09

0.035

0.030

Model 2: FGR‡ v non-FGR§

0.93

0.89–0.98

0.003

0.062

Model 2a: adjusted for child height

0.93

0.89–0.98

0.006

0.055

Model 2b: adjusted for child weight

0.95

0.90–0.99

0.028

0.033

Model 3: current height, cm

1.002

0.99–1.01

0.179

0.013

Model 4: current weight, kg

1.001

1.001–1.003

0.001

0.076

Model 5: body mass index

1.007

1.003–1.01

< 0.001

0.089

FGR = fetal growth restriction. * All models adjusted for gestational age, sex and contemporary age. † Difference between fully adjusted birth models with and without the measure of interest. ‡ Birthweight < 10th percentile for gestational age. § Birthweight ≥ 10th percentile for gestational age.

4 Size at birth and adolescent height and weight: relationships with fasting insulin concentrations (mU/L) among Aboriginal adolescents (n = 134)*

Model

Ratio

95% CI

P

R2†

Model 1: birthweight, kg

1.28

0.94–1.73

0.112

0.019

Model 1a: adjusted for child height

1.12

0.82–1.54

0.471

0.004

Model 1b: adjusted for child weight

0.87

0.66–1.15

0.326

0.005

Model 2: FGR‡ v non-FGR§

0.92

0.65–1.31

0.656

0.002

Model 2a: adjusted for child height

1.01

0.71–1.43

0.961

0

Model 2b: adjusted for child weight

1.27

0.94–1.71

0.120

0.012

Model 3: current height, cm

1.03

1.01–1.05

0.006

0.055

Model 4: current weight, kg

1.03

1.02–1.03

< 0.001

0.299

Model 5: body mass index

1.09

1.07–1.12

< 0.001

0.307

FGR = fetal growth restriction. * All models adjusted for gestational age, sex and contemporary age. † Difference between fully adjusted birth models with and without the measure of interest. ‡ Birthweight < 10th percentile for gestational age. § Birthweight ≥ 10th percentile for gestational age.

Specialists sign up to Indigenous initiative

The nation’s specialist medical colleges will upgrade their curricula and identify Aboriginal medical trainees under a landmark agreement struck with the peak body of Indigenous doctors.

The Australian Indigenous Doctors’ Association (AIDA) and the Committee of Presidents of Medical Colleges (CPMC) have signed a Collaboration Agreement that includes measures to support the training of Indigenous practitioners and to improve the ability of all doctors to work competently with Aboriginal and Torres Strait Islander people.

AIDA Chief Executive Officer Romlie Mokak told Australian Medicine that the Agreement was one of a number of formal partnerships recently developed by his organisation with peak medical education and training organisations.

The announcement came as the nation’s governments missed a deadline to renew their commitment to closing the health gap between Indigenous Australians and the rest of the community, heightening concerns that recent gains made will be squandered.

The nation’s first $1.6 billion, five-year National Partnership Agreement on Closing the Gap in Indigenous Health Outcomes expired in 30 June, and so far only the Commonwealth and Victoria have committed to a new five-year deal.

The failure of the many of the states to so far commit to a fresh Closing the Gap plan has come amid signs that an increasing number of Indigenous students are training to become doctors.

AIDA estimates there are currently around 175 Indigenous medical graduates and 300 Indigenous medical students.

Mr Mokak said that in the last two years Indigenous students had comprised 2.5 per cent of all medical school admissions, putting them at parity with their presence in the broader population.

“That would have been unheard of 10 years ago,” he said. “Over the next three to four years, as people graduate, we will see a steady rise in the number of Indigenous graduates.”

But Mr Mokak said increase in graduate numbers alone was not enough, and had to be accompanied by improved support for Indigenous students through pre-vocational and vocational training.

“Our focus is the whole continuum. We are not focused on a particular level of training or particular specialty,” he said. “Support for graduates at the junior doctor level is critical, [and] we want more people to know about pathways in specialist areas.”

 CPMC Chair Professor Kate Leslie said Aboriginal and Torres Strait Islander doctors were “significantly under-represented” in the medical workforce, and all 15 specialist medical college Presidents are committed to leading the change with our partners AIDA”.

Under the Agreement, the Colleges will collate data on the number of Aboriginal trainees and practitioners within their ranks, and every year each College will send either its President or Chief Executive to spend time at an Indigenous health service, to gain first-hand experience of the conditions and challenges faced.

Mr Mokak said that, just as important as encouraging more Indigenous people into medical training was efforts to improve awareness of Indigenous culture, society and outlook among the broader medical community.

To help achieve this, AIDA is working with each College to upgrade their curricula by “providing guidelines for each speciality of things in the training of your Fellows which we would think would be necessary to know,” he said.

Mr Mokak said these initiatives could serve as an example of how to achieve improvements across a wide range of areas, not just medicine.

“If we get this agenda right in medicine, we are sending a significant message to the rest of the health system that if doctors are able to tackle these issues, it should be the same for all health professions, and all professions more broadly,” he said. “We see this as not only important work for medicine, but important work for the whole country.”

Adrian Rollins

A time and a place

This issue of the MJA, timed to coincide with NAIDOC Week, is devoted to exploring the health status of Australia’s Aboriginal and Torres Strait Islander peoples — particularly our children and young people. Children aged 0–14 years make up 35% of the Australian Indigenous population, write Eades and Stanley. Data on their health and development are patchy but indicate a growing divide between Indigenous and other Australian children for several risk factors and conditions. Azzopardi and colleagues add a systematic review of the evidence for young people aged 10–24 years into the mix, finding gaps in the observational research for urban settings, mental health and injury, and confirming the well known dearth of interventional studies.

Two studies in this issue add to the scant evidence available by testing simple interventions that might lead to improvements, such as providing subsidised fruit and vegetable boxes to disadvantaged families in regional towns (Black and colleagues) and swimming pools in remote communities (Stephen and colleagues).

Turning our thoughts to the health needs of Indigenous children is always important but is particularly timely now. A federal election, with all its potential for policy upheaval, is just 2 months away. In the first article in our pre-election series, Arabena recognises an urgent need for better data to evaluate existing and future policies, and envisages a plan for health that takes Aboriginal and Torres Strait Islanders’ perspectives, wishes and culture into account, and brings an end to aspects of the health system that contribute to inequality, such as racism.

Independently of the election, the Australian Government is developing a new National Aboriginal and Torres Strait Islander Health Plan for the next decade. Kimpton, president of the Australian Indigenous Doctors’ Association, says the plan will have the best chance of success if it has at its heart some important principles: nurturing of the Indigenous health workforce; genuine, strong partnerships with Indigenous organisations; fostering culture as integral to health and wellbeing; and promoting Indigenous leadership, while involving the whole health system.

The solutions to many health problems for Indigenous children lie outside the health system, but making our health services accessible, culturally safe and appropriate places will lead to better outcomes for the families who inevitably need them. “Cultural competence” can be a daunting term for doctors. Thackrah and Thompson encourage us to look at our own culture of medicine and the practical realities of patients’ lives
when trying to put this difficult concept into practice.

Amid all this thinking and soul searching, there are good examples of what works — innovative health promotion and education programs combining the nurturing effects of “country” with exchanges of new knowledge (Webb and colleagues), and thriving health services where Indigenous families can truly have their health needs met and that also serve as centres of outreach bringing sorely needed medical expertise to remote communities (McGilvray).

As Milroy reminds us in her response to
a study that found many Aboriginal children had been exposed to traumatic, potentially health damaging experiences (Askew and colleagues), Indigenous children need access
to the best possible health services right now and for years to come.

History tells us that policies fail, and services falter, when they are not developed in consultation with those for whom they are designed. On this point, Eades and Stanley concur: “… we believe that Australian services have failed to close the gap in child health because they have been developed without involving or engaging First Nations people”. At this important time in Australian history, we have yet another chance to get it right. Be it by public policy or individual action, we need to do all we can to make our health services places of healing for Aboriginal and Torres Strait Islander children and their families.

Partnership and leadership: key to improving health outcomes for Aboriginal and Torres Strait Islander Australians

The Australian Indigenous Doctors’ Association urges all medical professionals to support and participate in the values it hopes will be embedded in future health policy

This year, we will see the development of a new National Aboriginal and Torres Strait Islander Health Plan to guide governments in improving the health of Aboriginal and Torres Strait Islander Australians.1 Development of the Health Plan will be led by the Minister for Indigenous Health, with the support of a stakeholder advisory group to bring together the government and organisations with expertise in Indigenous health.2

The aim of this Health Plan is to shape the tone, direction and content of Indigenous health policy into the future. Apart from becoming familiar with the evidence and government priorities on areas of Indigenous health that relate to our work, medical professionals should note the particular values and themes that the Australian Indigenous Doctors’ Association (AIDA) wants to see embedded throughout the document; these include culture, partnership, Indigenous leadership and workforce. These principles are inextricably linked and are important not only to federal policy development and implementation but also to individual medical professionals in a range of areas, including in our day-to-day interactions with patients, care planning and staff recruitment and development.

Workforce will need to be an important feature of the Health Plan because building an adequate health workforce is crucial to delivering high-quality, sustainable health services for Indigenous people. The Indigenous medical workforce in Australia is growing, but Indigenous people are still underrepresented in this area. In 2011, the intake of first-year Indigenous medical students in Australian universities reached parity at 2.5% — for the first time matching the proportion of Australia’s population made up of Indigenous people.3 To ensure that the Indigenous medical workforce continues to grow, academic, professional and cultural support is essential. In particular, Indigenous medical students and doctors are more likely to stay and thrive in learning and working environments that consistently demonstrate cultural safety.3

The solution to both a stronger workforce and further improvements in Indigenous health is partnership: our people working alongside non-Indigenous people in order to achieve an agreed goal. Such partnerships are seen in collaboration agreements which spread across the medical education continuum. Agreements currently exist between AIDA and Medical Deans Australia and New Zealand, and AIDA and the Confederation of Postgraduate Medical Education Councils; an agreement will soon be launched between AIDA and the Committee of Presidents of Medical Colleges. This collaboration did not happen overnight; it was a lengthy process, with trust being built over time and through each organisation demonstrating its commitment to improving Indigenous health. These best-practice models are available on the AIDA website (http://www.aida.org.au/partnerships.aspx) and should be recognised by all medical professionals as a best-practice framework for improving Aboriginal and Torres Strait Islander Health.

For Aboriginal and Torres Strait Islander peoples, health is not just about an individual’s physical wellbeing; it is a holistic concept that encompasses the social, emotional and cultural wellbeing of the entire community. AIDA asserts that the Health Plan needs to embed Aboriginal and Torres Strait Islander cultures at its centre in recognition of the importance of culture to the health and wellbeing of Indigenous people. As medical professionals, we must also embed culture in the provision of health services to Aboriginal and Torres Strait Islander people, as evidence shows correlations between increased cultural attachment and better health and wellbeing.1 In achieving this, it is important that the Health Plan

be developed and conducted through genuine partnerships between governments, Indigenous organisations and communities, not only because such an approach is consistent with what is contained in the United Nations Declaration on the Rights of Indigenous Peoples, but because it makes good sense.4

AIDA recommends creating strong partnerships with Indigenous organisations and communities to guarantee Indigenous participation in decision making and showcase strong Indigenous leadership in communities.3

Aboriginal and Torres Strait Islander leadership, particularly through the peak national health bodies, is paramount in providing government with professional advice from Indigenous health practitioners in developing the Health Plan.3 AIDA recognises that Aboriginal and Torres Strait Islander community-controlled health organisations play a central role in the health of Indigenous people; however, it is also important that members of the non-Indigenous mainstream health workforce play their role in delivering equitable services for Aboriginal and Torres Strait Islander people. It is expected that the National Aboriginal and Torres Strait Islander Health Plan will be released later this year. I encourage you, upon reading it, to ask yourself what your role is in delivering quality and culturally appropriate health care to Aboriginal and Torres Strait Islander people, and to consider how this role could be strengthened. As members of the health workforce, we need to locate ourselves within the Health Plan and implement strategies in partnership with Indigenous communities and organisations. AIDA argues that this combination of strategic action and partnership is critical to achieving equitable health and life outcomes for Aboriginal and Torres Strait Islander people.

Beyond cultural security; towards sanctuary

Building an oasis in the desert for the health and wellbeing of our children

The current state of Aboriginal and Torres Strait Islander health compared with the wider Australian population is well known, with most common health conditions overrepresented, a significant gap in life expectancy, and poorer physical and mental health outcomes. Aboriginal and Torres Strait Islander peoples continue to experience lower levels of access to health services, are more likely to be hospitalised for health conditions, suffer a greater burden of emotional distress than the rest of the population, and are overrepresented in regard to health risk factors such as smoking.1 With fewer elders and adults available to buffer families, children and young people often bear the burden of care for sick relatives and are more likely to experience the death of several family members during their developmental stages. Many families will experience multiple life stress events within a relatively short period of time, and the effects of this may be cumulative over generations.2 In a study in this issue of the Journal, Askew and colleagues found that urban Aboriginal and Torres Strait Islander children who had experienced significant life stress events had poorer physical health and more parental concern regarding their behaviour. Of note, 51% of the study participants reported experiencing at least one stressful event.3

Recently, the link between stress, development and poor health has been the focus of attention, with an emphasis on promoting good social and emotional wellbeing to enhance development and improve health outcomes. Within the health service environment, culturally appropriate, accessible and secure models of care have been developed to overcome health disparities. But is this extensive knowledge and increasingly sophisticated health system enough to reduce the burden of disease, disadvantage and distress? How can we bring all of this knowledge together to benefit the growth and development of children, enhance their wellbeing and reduce the propensity towards chronic disease and early death?

In the mental health field, the concept of trauma-informed care has gained momentum in assisting clinicians to better understand how trauma affects behaviour, recovery and responsiveness within clinical services. As noted by the Mental Health Coordinating Council, trauma-informed care attempts to create “an environment that is more supportive, comprehensively integrated, empowering and therapeutic”.4 This concept is even more important in regard to children, as we understand the profound impact that trauma can have on the developing brain, memory and self-regulation, as well as attachment relationships and physical health. So how can the health service environment maximise the opportunities to promote resilience, buffer the many traumas Aboriginal and Torres Strait Islander families will face, reduce the secondary impact of trauma in health services, and continue to improve health and wellbeing outcomes?

In 2011, as part of a Yachad Scholarship study tour in Israel, I visited several children’s trauma treatment programs and was impressed by the values and attitudes many of the programs had in common. These included believing each child had the capacity for positive change and recovery; the staff accepting both personal and professional responsibility for making the program work for the benefit of the child; having a collective responsibility for all of the nation’s children as “family”; having the resourcefulness and flexibility to make things happen if they would benefit the child, such as arranging for music lessons; and never giving up on a child. The belief was often expressed that after what some of these children had been through, they deserved the very best the service could offer. One of the residential services was set up as an oasis in the desert, a place of beauty and tranquillity, yet vibrant and full of life. It was a safe place to be, warm and comforting, but still able to lift you up to see the stars. Every component of the building, landscape and program design was aimed at promoting wellbeing, reducing secondary trauma, empowering recovery and restoring potential. Each child was given the opportunity to choose aspects of his or her treatment, and unique talents and life skills were identified, nurtured and strengthened.

Aboriginal and Torres Strait Islander families will continue to experience stressful life events and adverse health outcomes far in excess of the rest of the population for many years to come. Many children will spend a lot of time in health services, either as clients or with their families. The way children are supported and treated within health services can have a significant influence on their life outcomes, especially given the high burden of risk that is pervasive across the population. Are we, as those charged with providing for their health care needs, able to give them the very best we have to offer during their time with us, through both our professional relationships and the health service environments we provide? Can we continue to build a culturally secure, trauma-informed model of care and provide an oasis in the desert?