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Preference: Indigenous Health

1

Can sleep contribute to “closing the gap” for Indigenous children?

Relatively simple interventions could make a significant difference

The wellbeing of Australian Indigenous children has long been an issue of concern and the subject of numerous national partnerships, action plans and government policies. This is primarily because of the high incidence of health problems and academic deficits among Indigenous children in comparison with non-Indigenous children.1 The aim of these government policies is to bring about a general increase in Indigenous children’s health and academic outcomes. We propose that poor sleep health may be a significant and, to date, poorly addressed factor that should be considered within the discourse around closing the gap in the health and wellbeing of Indigenous children and young people.

The body of literature on this issue provides very clear evidence that sleep problems in children (whether they have a physiological or non-physiological cause) have strong and causal associations with secondary deficits in academic performance, attention and learning, emotional regulation, behaviour and mood regulation, with increased likelihood of obesity, diabetes, high blood pressure, somatic health and psychological health.2 While there is a paucity of comparable data for Indigenous children, some studies are beginning to report similar findings. Recent findings on the sleep of Indigenous children suggest that this group may also be encumbered with a higher prevalence of sleep problems.3–7

Among physiological sleep disturbances, secondary sleep disturbance due to asthma has been reported in non-Indigenous children, but has yet to be fully explored in Indigenous children. This is despite the greater incidence of asthma among Indigenous children compared with non-Indigenous children.4 Sleep disordered breathing (ranging from primary snoring to obstructive sleep apnoea accompanied by nocturnal hypoxaemia) has known associations with daytime deficits in neuropsychological and psychosocial domains, and has also been found in one study to have a prevalence of 14.2% in Indigenous children.3 This study, one of the first to investigate sleep-disordered breathing in Indigenous children, found high prevalences of snoring, wheezing and restless sleep. Despite this, no further studies have been undertaken since 2004.4 Associations between all these conditions therefore remain to be explored in Indigenous children.

Not only must we consider the physiological aetiology of poor sleep, but also the impact it has on both the physiological and psychosocial development of Indigenous children. Recent findings suggest links between obesity and reduced sleep duration,2 and with the increasing and worrying prevalence of obesity among Indigenous children in Australia, their sleep profiles should be considered. In addition, there is a growing body of research showing associations between diabetes and sleep quality that have not been sufficiently explored in Indigenous children and young people.8

Some efforts to understand sleep in Indigenous children have been undertaken. In summary, data from various studies show that, compared with non-Indigenous children, Indigenous children report poorer sleep quality (eg, sleep scheduling, sleep fragmentation),5,7 decreased sleep duration,7 worse sleep hygiene,5 increased sleepiness,6 and more instability and irregularity in their sleep–wake patterns,5 particularly in “get up” times. Furthermore, these sleep problems were related to aggression,6 withdrawn behaviours,6 thought problems and internalised behaviours,6 reduced reading ability and numerical skills.7

What now?

Poor sleep, whether inferior in quality or quantity, is essentially modifiable. There are currently few data on which to base any assessment of how much poor sleep might contribute to poor health, wellbeing and academic performance in Indigenous children, but evidence in non-Indigenous children and young people suggests that not only is it significant, but also that it is amenable to treatment regardless of whether the sleep problem has a physiological cause.2 Treatment can have significant and positive outcomes. Considering that sleep is one of the key requirements of good health, it is only logical that it should be explored, investigated and improved, and that doing this might have positive impacts on these children’s lives. This may seem simplistic, but health-related lifestyle interventions have been shown to be successful in the past.9 Such interventions can be targeted at an individual or community level, and if they have a positive impact on even a single child, this would be an improvement on what is happening at present.

Clearly, there are considerable challenges to intervening to try to close the gap between Indigenous and non-Indigenous health, including socioeconomic and demographic factors, cultural differences, preferences about sleep and sleep hygiene and parenting, and Indigenous scepticism about “white fella” interventions. However, exploring whether sleep interventions would be an acceptable method to bridge our divides might be worth the effort. Certainly careful and sensitive negotiations have previously allowed researchers to engage and work with community elders to facilitate the first objective investigation of children’s sleep in a remote Indigenous community.7

Poor sleep is inherently modifiable. Therefore, any contribution sleep has to downstream factors (eg, health, wellbeing, academic performance, behaviour) is also potentially modifiable. For this reason, research funding and cross-institutional and multidisciplinary research efforts into understanding Indigenous sleep are necessary if we are serious about investigating not if but how much sleep is a contributor to Indigenous wellbeing so we can attempt, through sleep, to close the gap.

Future initiatives to improve the health and wellbeing of Aboriginal and Torres Strait Islander peoples

Continuing to close the health gap will require innovation; long-term, systematic approaches that improve the quality and integrity of data; collaborations and partnerships that reflect an ecological approach to health, and recognition of the proper place and contribution of Aboriginal and Torres Strait Islander peoples in Australian society

At long last there are signs that the gaps between the health of Aboriginal and Torres Strait Islander people and non-Indigenous people are closing — but systematic, long-term action needs to continue both within and outside the health system to realise true health equality, and for us to know that we have achieved it.

According to the 2012 report of the Aboriginal and Torres Strait Islander Health Performance Framework, a number of positive trends in Aboriginal and Torres Strait Islander health include:

  • the mortality rate has declined significantly (by 33%) between 1991 and 2010 among people living in Western Australia, South Australia and the Northern Territory combined;

  • deaths due to avoidable causes decreased significantly in WA, SA and the NT combined, down 24% between 1997 and 2010;

  • deaths from respiratory disease decreased significantly from 1997 to 2010, and the gap with non-Indigenous Australians has also narrowed; and

  • mortality among infants aged less than 1 year declined by 62% between 1991 and 2010, perhaps reflecting the benefits of immunisation, improved access to primary health care services, the use of antibiotics and earlier evacuation to hospital for acute infections.1

Of course there remain areas where the gap persists or in some cases has grown, including chronic disease, injury, cancer, disability and low birthweight babies. It appears that in some areas (such as cancer) improvements in the quality, accessibility and impact of treatment are resulting in significantly improved death rates for non-Indigenous Australians, but Aboriginal and Torres Strait Islander people are missing out. The causes of this discrepancy seem to lie in disparities in stage at diagnosis, treatment received and survival rates.

Cutting across these trends are persistent gaps in the quality of data. Our inability to know whether large investments made in recent years in Aboriginal and Torres Strait Islander health are paying off should be a major focus for future strategies. In general, our population does not seem to be benefiting from the same level of sophisticated population-level tracking, health assessment or data integrity that majority populations take for granted.2 Good data are crucial, not just to know the impact of what we have done, but to guide what we are doing.

In this context it is pleasing to see the recent process of developing a new national plan to guide future investments in Aboriginal and Torres Strait Islander health, developed through a collaborative process including Aboriginal and Torres Strait Islander peak bodies, communities, services, researchers, advocates and clinicians.3 The new national plan needs to set directions for the next 10 years and expand and align with an ecological view of health, include concepts important to Aboriginal and Torres Strait Islander peoples and influence other sectors that affect health, such as education, employment, housing and early childhood development. This multifocal approach could have implications for the design, implementation and evaluation of projects, and will necessitate a reconceptualisation of partnerships and collaborations, while fostering innovations and knowledge exchange.

Finally, we will need to redress some of the less palatable aspects of the health system that contribute to inequality, such as racism.4 Embodied in dubious practices, disparities in access and subtle variations in effort within health and other institutions and programs, racism has had and continues to have a real and damaging impact on the health of Aboriginal and Torres Strait Islander people. It is clear that full health equality cannot be achieved until racism and other practices that deny our status and rights as the original and First Peoples of Australia can be overcome. My hope is that not only do we redress racism in health and other systems, but that this nation recognises and enables each and every Aboriginal and Torres Strait Islander person the opportunity to rise to the full potential of our existence.

Refining the concept of cultural competence: building on decades of progress

The impact of culture in the clinical encounter is recognised as a contributing factor to patterns of health service utilisation and is a key focus of cultural competence training.1,2 While some studies have identified beneficial effects of cultural competence on health professionals’ knowledge, attitudes and skills, and on levels of patient satisfaction, few have explored its effects on health outcomes. This is unsurprising given that the factors affecting health outcomes are numerous and complex. The Commission on Social Determinants of Health has noted that health inequalities are largely related to the circumstances of people’s lives and to the services available to treat illness.3 In turn, people’s circumstances and the health care system are shaped by social, political and economic realities. Cultural knowledge is embedded in these circumstances and realities, and helps frame patients’ explanatory models of illness and clinicians’ decision making.2 It has been argued, however, that these two world views can collide in the clinical encounter.4 Cultural competence training aims to improve the quality of health care and reduce health disparities by focusing on communication and trust between patients and health care providers and enhancing provider knowledge about sociocultural factors linked to health beliefs, practices and utilisation of services.5

The idea of educating health professionals to be culturally competent began in earnest in the United States in the 1990s. The term “cultural competence” first emerged in the late 1980s and was defined as “a set of congruent behaviors, attitudes, and policies that come together in a system, agency or amongst professionals and enables that system, agency, or those professionals to work effectively in cross-cultural situations”.6 Cultural competence in health care was described as an emerging field in the US in 2002; however, over the past decade it has become firmly embedded in professional accreditation standards.7 In Australia, health professional competencies consistently make reference to cultural competence,8,9 and the concept has received legitimacy with its incorporation into significant health policy documents.10–13

While strategies associated with cultural competence aim to make services more accessible for patients from diverse cultural backgrounds, more recently they have focused on specific groups, particularly Indigenous Australians, where the failure of services to address large disparities in health outcomes is stark and confronting. Connecting Indigenous patients with the health system and communicating effectively can be challenging and has often not been done well (Box 1 and Box 2). Indigenous cultural competence has been identified as a desirable attribute of Australian health professionals.13–18 Perhaps as a result of the plethora of alternative concepts such as cultural safety, cultural awareness and sensitivity, cultural security and humility, and more recently cultural literacy, the use of an overarching term was inevitable, despite most concepts having different frames of reference.17,19 Cultural competence strategies usually target the health workforce with the aim of improving the interactions between the patient, the provider and the health care system, as the intermediate step to improving health care utilisation, service delivery and health outcomes. Many aspects of this concept remain the subject of debate.

Social science perspectives

Limitations of cultural competence highlighted by social scientists working in clinical and academic settings largely fall into three categories: lack of clarity around the concept of culture, inadequate recognition of the “culture of medicine” and the scarcity of outcomes-based research that provides evidence of efficacy in improving health.

Unpacking culture

While it is recognised that a patient’s cultural background may be significant in clinical encounters, lack of clarity about the concept of culture can distort its impact.2,4,20–22 Anthropology, the discipline from which the term “culture” originated, offers many definitions but most make reference to a system of shared meanings or guidelines that are inherited and provide a lens through which to view the world. Contemporary anthropologists stress variations that exist across cultures with respect to beliefs, practices, norms, behaviours and expectations. Helman, for example, notes that culture is “an increasingly fluid concept, which in most societies is undergoing a constant process of change and adaptation”.20 Social scientists stress that cultures are complex, heterogeneous and dynamic, and intricately connected to the social context of people’s lives.2,4,21,22

So how does this understanding of culture differ from its usage in medical settings? Critiques from social scientists suggest that culture is often conflated with race and ethnicity, resulting in reification of existing racial categories.4 Central to this criticism is the failure to recognise diversity within cultures and the concomitant reductionism whereby culture is identified as a variable associated with essential differences between groups. Culture is viewed as a “risk factor” and cultural attributes as potential sources of the problem. Kirmayer noted that culture has been framed in terms of “ethnoracial blocs” which “conflate language, geographic origin, ethnicity and race” and “do not capture the diversity of society and the rapidly growing numbers of people who define themselves in hybrid ways that cut across these categories or escape them entirely”.21 Cultural competence literature tends to associate culture with group membership and shared beliefs and values that influence behaviour in health care settings.21 Not only does this approach underestimate cultural diversity within groups, but the process of “essentialising” culture removes individuals from their complex social worlds in which the structural and material determinants of inequality may be as powerful as cultural influences on health inequity. In an attempt to provide more conceptual clarity around cultural competence, Lo and Stacey coined the term “hybrid habitus” which interprets patients’ cultures as “the broad, less than fully conscious cultural orientations that shape a patient’s sense-making in clinical settings . . . [and] in turn, are shaped by surrounding, intersecting structural forces”.22 These forces may include socioeconomic status, gender, language and experiences of racism, all of which can interact with cultural orientations and influence the clinical encounter. This deeper understanding of culture in all its complexity has practical implications in health care settings. A patient’s culture is not reduced to stereotypical attributes, but rather understood as comprising layers of meaning that extend beyond values, beliefs and practices and are shaped by and in turn shape social structures.

However, any examination of the meaning and use of “culture” needs to consider the culture of medicine itself to assess its role in reproducing or addressing health inequities.

Culture of medicine

In the US, Good and colleagues questioned why disparities in health care continue to exist despite the introduction of cultural competence training in health professional programs.23 They suggested the need for a critical analysis of the culture of medicine where the “social processes within our complex medical institutions” are explored, including the presence of institutional racism, power imbalances and the role of professional socialisation. Taylor reinforces this, noting that cultural competence strategies have an overemphasis on the patient’s culture with scant attention paid to the culture of biomedicine.24 Institutional and professional medical culture is characterised by expert language and efficiency in clinical decision making based on legitimate medical knowledge. Taylor suggests that “it is confidence in the truth of medical knowledge that underwrites physicians’ special power to alleviate suffering”. Medical knowledge is thus not seen as a cultural product but as “real” knowledge which leads her to describe medicine as “perceiving itself to be a ‘culture of no culture’ ”.24 While some may disagree with this, it has consequences for the development of cultural competence curricula that “go beyond focusing on ‘other’ cultural groups, and attend to cultural dimensions of medicine itself”. Central to this discussion is the potential mismatch between professional medical socialisation, institutional practices and cultural competence strategies. Indeed, clinicians sometimes can be at odds with institutional directives and feel constrained by administrative practices that may compromise patient care.

Despite cultural competence training becoming commonplace in medical programs in Australia and elsewhere, few studies have focused on the culture of medicine itself. As Good et al note “rarely do students have the time or the formal sanction to critically analyze the profession and institutions of care to examine how treatment choices, quality of care and research practices are shaped; or how medical culture may produce processes that evolve into institutional racism . . . in clinical practice”.23 Kleinman and Benson go further, suggesting that the culture of biomedicine is “key to the transmission of stigma, the incorporation and maintenance of racial bias in institutions, and the development of health disparities across minority groups”.2 Implementing a more expansive notion of cultural competence that incorporates greater critical analysis of biomedicine has potential for less discordance between institutional culture and strategies aimed to improve culturally informed care.

Problems of measurement and limited outcomes-based research

Finally, critiques of cultural competence by social scientists and others have drawn attention to inadequate measures of the concept and the scarcity of outcomes-based research that links cultural competence strategies to better health.25–30 A study of quantitative measures of cultural competence found many hidden assumptions in survey questions designed to assess the impact of educational interventions, including the notion that frequent contact or immersion experiences necessarily enhance competence.29 Much depends on the kinds of interactions and the quality of the experiences, with contact alone not necessarily fostering insight. Recent studies also have found a lack of rigorous evaluation of cultural competence measurement tools, with few instruments having been validated. Chun noted that cultural competence training is often viewed as “unscientific” due to inadequate measurement techniques that can undermine implementation efforts.27 This is reinforced by findings of a review of the methodological rigour of studies evaluating cultural competence, which found a consistent lack of rigour, the consequence of which “limits the evidence for the impact of cultural competence training on minority health care quality”.26 In addition to rigorous instrument evaluation, qualitative methods, including observations, interviews and reflective journals should supplement traditional survey techniques when determining the effectiveness of cultural competence training.29

The first systematic review of studies assessing whether educational interventions to improve cultural competence were linked to improvements in health outcomes concluded that where an association was established, it tended to be in a positive direction.28 However, the authors identified many methodological limitations of existing studies and drew attention to the overall paucity of high-quality research, concluding that the evidence was not robust. Looking ahead, they noted that “subjective constructs such as patient trust and the quality of the patient experience using validated measures have emerged as outcomes of intrinsic value that should also be considered in the cause-effect dynamic”.28 Inherent in cultural competence measurement issues is the question of who decides whether a health professional has achieved cultural competence; arguably, the patient as the recipient of services is best positioned to make this judgement. The authors noted that because educational interventions are often removed from clinical outcomes, other measures such as enhanced trust between patient and practitioner and a high degree of satisfaction with a clinical encounter are worthy outcomes in health care settings and may also contribute to improved levels of utilisation.28

Conclusion

Social science critiques of cultural competence highlight the lack of conceptual clarity around the use of the term “culture” in clinical encounters, inadequate recognition of the “culture of medicine” and a scarcity of outcomes-based research that provides evidence of efficacy in improving health.

The value of training in cultural competence as an educational intervention will ultimately be validated by enhancing access to and achieving equity of health services and better health outcomes for culturally diverse groups. Given strong evidence that inequities in health arise from inequities in society, cultural competence strategies should not be divorced from addressing the material circumstances of people’s lives, an issue pertinent to the oldest and newest inhabitants of Australia. Perhaps there are unrealistic expectations about what culturally informed health care delivery can achieve in the absence of systematic attention to the structural and financial impediments to implementing the professional advice provided in health encounters. A nuanced and sophisticated understanding of “culture” in clinical settings would be a useful start to discerning the role that cultural competence plays in reducing health disparities in minority groups.

1 No wonder people don’t come back*

One of the Aboriginal doctors was doing a paeds [paediatrics] trip and a patient had been driven overnight from Wiluna. And the doctors barely had time to see them [the family] and then they did not make them welcome, so this Aboriginal doctor was horrified. No wonder people don’t come back. It is the same with ordinary appointments. The reason why people miss appointments is because they can’t see the value of them. And I’ll ask them what happened at their outpatient appointment and they’ll say “They did what you do”. “What did they say?” “They said they will write you a letter”. “Did they examine you?” “Not really”. So there is a sense that these appointments are futile, especially the follow-up ones.

The young doctors that see the patients are afraid to discharge them from the clinic and so when they see them and everything is the same, they rebook them for another appointment for no good reason except they are too nervous to say “you don’t need to come back”.

It is a hassle to get a babysitter for your six kids, find transport, wait 4 hours . . . for nothing.

* Transcript notes from an interview with an experienced general practitioner who works at an Aboriginal Medical Service. The GP describes the lost time and opportunity costs for patients travelling
great distances for appointments that may be very brief and perhaps
not even necessary.

2 The heart of the matter*

Another thing is patients are not told enough; it’s a bit of a paternalistic attitude that doctors have anyway, and even more so with Aboriginal patients, they are not given enough information. One story is of a patient who told me he loved this private cardiologist and I was amazed. I couldn’t understand why, because this guy was as rough as guts and the doctor was a posh three-piece suit sort of guy . . . When I asked him he said because the doctor had a fabulous model of a heart and he shows me everything, you know. He just thought that guy was the bee’s knees . . . he took the time to show him pictures of his arteries . . .
so taking the time to show people with models and trying to explain what you’re doing is just fundamental . . .

Of course it’s hard in hospitals because doctors have so little time; but if they don’t explain things properly and patients don’t take their tablets because things aren’t clearly explained then they are wasting their time anyway.

* Transcript notes from an interview with an experienced general practitioner who works at an Aboriginal Medical Service. This excerpt highlights good communication and its importance in breaking down barriers between patient and clinician.

How will we close the gap in smoking rates for pregnant Indigenous women?

Antenatal smoking is the most important modifiable cause of adverse pregnancy outcomes.1 Indigenous Australian women are more than three times more likely to smoke during pregnancy than non-Indigenous women.2 As a result, adverse outcomes are more frequent in Indigenous than non-Indigenous babies, with smoking as an independent risk factor.3

Reviews of antenatal smoking interventions have shown effective cessation strategies for pregnant women.1 However, persistently high rates of smoking during pregnancy among Indigenous women suggest that current interventions have had limited impact. Finding ways to effectively reduce smoking in pregnant Indigenous populations is a high priority. Previous systematic reviews have examined smoking cessation interventions for Indigenous peoples; however, none has specifically investigated smoking cessation among pregnant Indigenous women.4,5

We undertook a systematic review to examine the effectiveness and methodological quality of smoking cessation interventions targeting pregnant Indigenous women. In December 2012 we searched MEDLINE, PsycINFO, CINAHL (Cumulative Index to Nursing and Allied Health Literature) and Cochrane databases with appropriate search terms, and checked reference lists of retrieved articles. Papers were included if they reported a smoking cessation intervention aimed at pregnant Indigenous women, included a control group and provided cessation results specifically for pregnant Indigenous women. Only peer-reviewed, English-language papers were included. We extracted data and assessed methodological quality against Effective Practice and Organisation of Care quality criteria.6

Of 59 identified papers only two met eligibility criteria: one from the United States with Alaskan Native women,7 and one from Australia with Aboriginal and Torres Strait Islander women.8 Both involved culturally tailored interventions specifically developed for the target group, and used face-to-face counselling, structured follow-up, attempts to involve family members and nicotine replacement therapy (NRT). Both studies found no treatment effect and had a number of limitations (Box).

This lack of evidence of effective smoking cessation interventions for pregnant Indigenous women prevents implementation of evidence-based programs and highlights a critical need for methodologically rigorous testing of possible strategies.

What interventions should we test?

Evidence from research with Indigenous populations, and with pregnant women generally, provides guidance about the strategies that hold promise for pregnant Indigenous women. These strategies are outlined as follows.

Tailor interventions to local culture

Interventions for Indigenous people need to be culturally secure and locally tailored in order to increase acceptability and accessibility.4,5,9 Involving local people in developing and tailoring intervention resources to the local context is critical for improving cultural appropriateness, building ownership and enhancing a sense of autonomy, all of which are important in successful cessation.10

Include routine assessment and support

Smoking cessation guidelines for pregnant women recommend a systematic approach to cessation where every woman is asked about her smoking status, with smokers followed up and supported to quit in a respectful manner.11 Health professionals may be reluctant to repeatedly assess smoking status due to concerns that it may be deleterious to their relationship with women and the women’s engagement with care.9,12–14 However, most Indigenous women expect antenatal care to include smoking cessation advice.15 Systems to support routine assessment and support should be included in intervention trials.

Provide relevant information

Indigenous women’s knowledge of specific risks of smoking while pregnant is often vague.9,15,16 Providing information on the harms of smoking and benefits of cessation may motivate some women to attempt to quit. Discussing the woman’s role as a mother and a role model for her family may be more motivating for some Indigenous women than health risk narratives and should be addressed in intervention trials.

Deliver cessation support through all antenatal providers

Overall, 78% of Indigenous women attend five or more antenatal visits during their pregnancies.2 Providing cessation support through routine antenatal care overcomes barriers to attending separate services.13 A collaborative approach between midwives, Aboriginal Health Workers (AHWs) and doctors, all providing consistent advice and support, will reinforce the importance of cessation. The credibility of medical practitioners may be a significant motivating factor for some women. In cases where midwives provide much of the care, the close relationship and frequent contact allows ongoing support. AHWs’ cultural knowledge and strong links with local families will enhance implementation of cessation support.14 In a survey of Indigenous women, over 70% of women felt that support from these professionals was likely to be helpful.17

Involve other members of the community

The high prevalence of smoking in Indigenous communities has resulted in smoking being “normalised” as a socially acceptable behaviour, with frequent triggers to smoke and cigarettes being readily available.9,16,18 Smoking is important in social relationships, and cessation can lead to feelings of isolation.18,19 Supportive environments for quitting have aided cessation among Indigenous ex-smokers.10 Trialling interventions that incorporate mechanisms to provide a supportive, pro-cessation environment, such as involving household members in supporting women, peer support groups and whole community interventions should be further explored.20

Address relapse

Interventions that incorporate strategies to prevent smoking relapse result in fewer women relapsing in late pregnancy.1 Up to 80% of women who quit during pregnancy relapse within 1 year.21 Specific relapse prevention support should be provided during pregnancy and postpartum, including information about the effects of environmental tobacco smoke on the baby, support to make a smoke-free home and support for household members to quit smoking.21 Relapse prevention strategies have not been examined among Indigenous women and should be included in future trials.

Use contingency-based financial rewards

Systematic reviews of antenatal smoking cessation interventions have found that financial rewards contingent on successful smoking abstinence are significantly more effective than other interventions.1 However, their efficacy with Indigenous women has not been tested. Australian surveys indicate that contingency-based rewards are considered likely to be helpful by over 90% of Indigenous women and 83% of their antenatal providers.17,22 This approach should be further explored with Indigenous women.

Other substances

Surveys of pregnant Indigenous women found that tobacco smokers were more than three times more likely than non-smokers to report cannabis or alcohol use, both of which are risk factors for continued smoking.17 Given the known negative impact of these substances on birth outcomes and the interaction between their use and use of tobacco, interventions should include explicit assessment of other substance use, with support to address these if required.11

Training providers

A lack of protocols and poor smoking cessation support skills have been identified as barriers to providing cessation support to pregnant Indigenous women.12 Well defined protocols detailing specific procedures, and the role of each provider, may assist in increasing provision of support in routine care.13 Training should cover skills in smoking cessation support, supportive communication and using protocols, as well as recording women’s smoking status, cessation behaviour and support provided, to facilitate consistent advice from all team members.

Possible challenges

Conducting complex behavioural intervention trials is difficult. Potential challenges include:

Random allocation

As smoking cessation support is provided at both the service and individual level, randomisation at the individual level is inappropriate as contamination between groups is likely. Cluster randomised controlled trials with randomisation of dispersed services may reduce this problem but require larger sample sizes and more participating services, increasing costs and logistics challenges. As services and communities may not be willing to be randomly allocated to “usual care”, it may be more appropriate to undertake a head-to-head comparison of two approaches considered likely to be effective.23

Adherence to protocols

Poor adherence to intervention protocols may occur as a result of unsuitable intervention requirements, inadequate staff training, high staff turnover and lack of systems to support the intervention. Smoking among AHWs has also been identified as a potential barrier to implementation and would need to be addressed as part of the intervention.14,16 Strong organisational support for the implementation and evaluation of strategies is critical to supporting adherence. Collaborative development of the intervention and study design with Indigenous services and pilot studies to assess acceptability and feasibility of the research will help successful implementation.

Conclusions

Given the importance of finding effective strategies to decrease smoking among pregnant Indigenous women, and the current lack of evidence to guide this process, there is an urgent need for rigorous studies to test innovative approaches. While there are many challenges in this research, these may be managed with existing methods for testing complex interventions in diverse settings.24 Without an evidence base, we risk implementing ineffective strategies, failing to improve outcomes and wasting scarce resources.

Quality rating of eligible studies reporting smoking cessation interventions aimed at pregnant Indigenous women, according to Effective Practice and Organisation of Care quality criteria6

Criteria

Patten et al7

Eades et al8

Design

Clinical controlled trial

Randomised controlled trial

Allocation sequence adequately generated?

Unclear

Low risk

Concealment of allocation?

Unclear

Low risk

Baseline outcome measurements similar?

Low risk

Unclear

Baseline characteristics similar?

Low risk

Low risk

Incomplete outcome data adequately addressed?

Unclear

Low risk

Knowledge of allocated interventions prevented?

Unclear

Unclear

Protection against contamination?

High risk

High risk

Selective outcome reporting?

Low risk

Low risk

Free from other risk of bias?

High risk

Low risk

Comments

The low consent rate and the fact that many women did not take part because they were
not ready to quit increases the chances of selection bias. The focus of the study was on feasibility and acceptability rather than on outcomes, although outcomes are reported

High loss to follow-up (33%), but this did not differ
between the groups. Randomisation was by week of
first visit, so the staff who were recruiting the women
were aware of the group allocation. This may have
contributed to the greater numbers recruited to
the intervention group

Urban Aboriginal and Torres Strait Islander children’s exposure to stressful events: a cross-sectional study

Adverse life events and chronic stressors experienced during early childhood can negatively affect development.1,2 While some exposure to stressful events can foster resilience,3 exposure to strong, frequent or prolonged stressors in childhood can result in dysregulation of physiological stress response systems,2,4 which can negatively affect the development of social and emotional wellbeing, behaviour, literacy, and physical and mental health.2,4,5 With the strong association between racial inequalities in health and chronic stress,6,7 the inequalities experienced by Aboriginal and Torres Strait Islander peoples compared with non-Indigenous Australians need to be considered in this context.

Aboriginal and Torres Strait Islander peoples experience higher rates of stressful events than the general population, which can, in part, be attributed to the lasting impact of colonisation, intergenerational trauma and ongoing experiences of disadvantage and exclusion.7–9 The 2010 General Social Survey found that 61% of Australians aged ≥ 18 years had experienced at least one stressful event during the preceding year.10 In comparison, the 2008 National Aboriginal and Torres Strait Islander Social Survey (NATSISS) found that 77% of Indigenous adults and 65% of Indigenous children aged 4–14 years had experienced at least one stressful event,11 and the Western Australian Aboriginal Child Health Survey (WAACHS) found that 71% of children had experienced at least three significant stressors.12 All three surveys used a checklist of negative life events to identify stressful events experienced in the previous year.

Indigenous children living in urban areas experience higher rates of stressful events than their counterparts in rural or remote areas.11,12 However, there is little research investigating their health status, despite the majority of Indigenous Australians living in urban settings and the different social and cultural milieus associated with these communities.13,14 We aimed to determine the frequency and types of stressful events experienced by urban Aboriginal and Torres Strait Islander children, and to explore the relationship between these experiences and the children’s physical health and parental concerns about their behaviour and learning ability.

Methods

This cross-sectional study used data collected during annual child health checks (CHCs) at the Inala Indigenous Health Service (IIHS) in Brisbane. The CHC is a comprehensive health assessment that aims to increase access to preventive health care.15 The IIHS, a Queensland Government general practice service,16 had 867 children listed as regular patients at the time of the study.

We recruited a consecutive sample of children aged ≤ 14 years presenting for CHCs between March 2007 and March 2010, whose parents or carers consented to the CHC information being used for research. Most children had one CHC during the study period; for those who had two or more CHCs, only data from the first visit were included.

Parents or carers were asked if any stressful events had occurred in the family that may have affected the child. Responses to this question were not limited by a time frame of when the events occurred or by use of a checklist of negative life events.

Parents or carers were also asked if the child had a history of chest, ear or skin infections, or injuries or burns, and if they had concerns about the child’s behaviour or learning ability. For school-aged children, parents or carers were asked to compare the child’s school grades to average. The child’s weight and height were measured and body mass index (kg/m2) was calculated. Family groupings of children were identified post-hoc by matching children’s surnames, addresses, known siblings, household size, presentation on the same day for a CHC, or the same stressful events being recorded.

We categorised the reported stressful events and calculated the proportion of children affected by each category of stressor. Using Stata, version 10.0 (StataCorp), we tested for relationships between reported stressful events and the independent variables using binary generalised estimating equation (GEE) methods, nesting children within families, employing exchangeable correlation structures and robust estimators of variance. A two-sided significance level (α) of 5% was used to define statistical significance.

Ethics approval was obtained from the University of Queensland’s Behavioural and Social Sciences Ethical Review Committee and the Metro South Human Research Ethics Committee. The Inala Elders Aboriginal and Torres Strait Islander Corporation supported the project, and results were disseminated back to the Inala Aboriginal and Torres Strait Islander community.

Results

Of the 541 children having CHCs in the study period, parental or carer consent to participate in research was gained for 432 (80%), and 344 (64%) were eligible for this study. These 344 children had a mean age of 7.3 years and were from 247 families. Most children were Aboriginal (312; 91%) and lived with at least one parent (286; 83%) (Box 1). Household size ranged from two to 11 usual members, with a median of five. No sibling was identified for 177 participants (51%); 50 participants (15%) had one sibling, 13 (4%) had two siblings, and seven (2%) had three siblings.

Of the 344 participants, 175 (51%) had experienced stressful events. There were no significant differences in the reported exposure to stressful events between sexes or age groups. Children from single-parent households or with teenage or unemployed parents were also no more likely to have been affected by stressful events than their counterparts (Box 1).

Categories of reported stressful events are shown in Box 2. Of the 175 children who had ever experienced stressful events, 42 (24%) had been affected by conflict in the family, 40 (23%) by the death of a family member or close friend, and 27 (15%) by housing issues, including overcrowding or housing insecurity. Violence or abuse, including domestic violence, had been witnessed by 20 (11%) and personally experienced by 18 children (10%).

Children affected by stressful events were more likely to have parents or carers concerned about their behaviour (P < 0.001) and to have a history of ear (P < 0.001) or skin (P = 0.003) infections (Box 3).

Discussion

About half of the children in this study had ever experienced stressful events. Strong associations were seen between stressful events and a history of ear and skin infections, and parental or carer concerns about the child’s behaviour. No significant differences were seen in the reported exposure to stressful events by individual or familial characteristics.

Compared with the urban Aboriginal and Torres Strait Islander children included in the NATSISS and the WAACHS, our study found a lower rate of stressful events and the absence of some expected stressors.11,12 None of our participants reported racism, trouble with the police or unemployment as stressors, whereas 12%, 16% and 32% of NATSISS respondents, respectively, reported these. In our study, 65% of parents or carers were unemployed, compared with a background unemployment rate for Aboriginal and Torres Strait Islander adults living in Inala of 24% in 2006, and rates of 11% in the broader population of Inala and 4% across Brisbane.17 It is possible that the common experience of unemployment has resulted in it becoming normalised in this group and therefore not considered stressful. However, it may also be an underlying but unacknowledged or unrecognised cause of other stressors such as familial conflict, illness or housing insecurity.

Our study has both strengths and limitations. We used routinely collected clinical data from children attending the health service, thus minimising inconvenience for study participants. Our 344 participants represented 64% of children having CHCs at the IIHS in the study period, and 40% of active patients aged ≤ 14 years. Issues such as the sickness of the presenting child or time constraints of the parent, carer or clinic staff could affect the number of CHCs conducted. Nonetheless, despite our clinic population comprising only 0.8% of Australia’s urban Indigenous children, our service completed 10% of the CHCs done in Australian metropolitan areas to June 2009.15

Our open-ended enquiry about types and frequency of stressful events introduces the potential for recall bias and underreporting. However, such enquiry is likely to elicit events that were particularly notable for the child and family.18 The open-ended nature of the enquiry also precluded assessment of a dose–response relationship between exposure and outcomes, and the cross-sectional nature of the data prevented any determination of causality between exposure and outcomes. The lack of a time frame associated with the reported stressful events also prevents establishing a temporal relationship between exposure and outcome.

Finally, this study represents one urban Indigenous context and may not be generalisable to other urban areas or Indigenous primary health care services, although there is little reason to assume there would be substantial differences in the results.19 These limitations do not negate the seriousness of our findings that about half the children were reported to have been affected by stressful events, and the significant association of this with poorer physical health and parental concerns about behaviour.

As childhood exposure to stress affects future health and wellbeing, longitudinal research is necessary to disentangle the causes and effects of stressful events. Health care services need to respond to any disclosure of stressful events by providing access to appropriate medical, psychological or social interventions, preferably through “in house” health professionals or referral to culturally competent community agencies. However, simply treating the impact of stressful events is insufficient without also dealing with the colonial legacy of displacement, child removal, marginalisation and exploitation that contributes to the excessive rates of transgenerational trauma and socioeconomic disadvantage experienced by Aboriginal and Torres Strait Islander peoples.9,20 The risk of not addressing both the causes and the effects of childhood exposure to stressful events is that the disparity in life expectancy between Indigenous and non-Indigenous Australians is unlikely to improve.8,9

1 Individual and familial characteristics of children having child health checks at Inala Indigenous Health Service, March 2007 – March 2010, by experience of stressful events

At least one stressful event

Characteristic

Overall (n = 344)

Yes (n = 175)

No (n = 169)

P*

Sex

0.40

Male

180 (52%)

94 (54%)

86 (51%)

Female

164 (48%)

81 (46%)

83 (49%)

Age (years)

0.45

≤ 4

107 (31%)

52 (30%)

55 (33%)

5–9

142 (41%)

78 (45%)

64 (38%)

10–14

95 (28%)

45 (26%)

50 (30%)

Ethnicity

0.96

Aboriginal

312 (91%)

157 (90%)

155 (92%)

Torres Strait Islander

7 (2%)

5 (3%)

2 (1%)

Both Aboriginal and Torres Strait Islander

25 (7%)

13 (7%)

12 (7%)

Main carer with whom the child lives†

0.07

Parent(s)

286 (84%)

137 (80%)

149 (89%)

Grandparent(s)

15 (4%)

8 (5%)

7 (4%)

Other relative(s)

20 (6%)

15 (9%)

5 (3%)

Friend(s)

1 (0.3%)

1 (1%)

0

In care

17 (5%)

11 (6%)

6 (4%)

Single-parent household‡

0.10

Yes

151 (44%)

87 (50%)

64 (38%)

No

192 (56%)

87 (50%)

105 (62%)

Employment status of parent(s)/carer(s)‡

0.10

Employed

121 (35%)

49 (28%)

72 (43%)

Unemployed

222 (65%)

125 (72%)

97 (57%)

Teenage parent(s)‡

0.23

Yes

14 (4%)

9 (5%)

5 (3%)

No

329 (96%)

165 (95%)

164 (97%)

* Calculated using binary generalised estimating equation methods, clustering children within their families. † Three observations missing from the group exposed to stressful events, and two from the group not exposed. ‡ One observation missing from the group exposed to stressful events.

2 Frequency of stressful events reported by parents or carers during child health checks for children who had experienced at least one stressful event (n = 175)

Stressful event category

No. (%) of children

Conflict in the family

42 (24%)

Death of family member or close friend

40 (23%)

Parental divorce or separation

28 (16%)

Housing issues (including overcrowding and housing insecurity)

27 (15%)

Lack of emotional support from parents

26 (15%)

Serious illness in the family

23 (13%)

Witness to violence or abuse (including domestic violence)

20 (11%)

Experienced abuse or violent crime (including domestic violence)

18 (10%)

Living away from parents, with other family members

17 (10%)

In foster care

16 (9%)

Alcohol or drug-related problem in the family

13 (7%)

Problems at school

11 (6%)

New to community

10 (6%)

Family member in prison

7 (4%)

Other

11 (6%)

3 Parental concerns about children’s behaviour and learning ability and physical health of children, by experience of stressful events

At least one stressful event

Variable

Overall

Yes

No

P*

Behaviour and learning ability

Parents or carers concerned about behaviour†

234

124

110

< 0.001

Yes

69 (29%)

50 (40%)

19 (17%)

No

165 (71%)

74 (60%)

91 (83%)

Parents or carers concerned about learning†

236

126

110

0.10

Yes

75 (32%)

47 (37%)

28 (25%)

No

161 (68%)

79 (63%)

82 (75%)

School grades on report card†‡

193

95

98

0.19

Below average

36 (19%)

24 (25%)

12 (12%)

Average or above average

157 (81%)

71 (75%)

86 (88%)

Physical health

Body mass index (BMI) category†

292

151

141

0.62

Overweight or obese (BMI > 25 kg/m2)

75 (26%)

37 (25%)

38 (27%)

Normal or underweight (BMI ≤ 25 kg/m2)

217 (74%)

114 (75%)

103 (73%)

History of chest infections†

308

156

152

0.10

Yes

33 (11%)

23 (15%)

10 (7%)

No

275 (89%)

133 (85%)

142 (93%)

History of ear infections†

313

160

153

< 0.001

Yes

87 (28%)

58 (36%)

29 (19%)

No

226 (72%)

102 (64%)

124 (81%)

History of skin infections†

308

158

150

0.003

Yes

67 (22%)

48 (30%)

19 (13%)

No

241 (78%)

110 (70%)

131 (87%)

History of burns or injuries†

306

153

153

0.51

Yes

42 (14%)

25 (16%)

17 (11%)

No

264 (86%)

128 (84%)

136 (89%)

* Calculated using binary generalised estimating equation methods, clustering children within their families. † Denominators shown for each variable differ due to varying numbers of missing observations. ‡ For school-aged children (5–14 years).

Impact of swimming on chronic suppurative otitis media in Aboriginal children: a randomised controlled trial

Rates of chronic suppurative otitis media (CSOM) among Aboriginal children living in remote areas in Australia are the highest in the world.1,2 A survey of 29 Aboriginal communities in the Northern Territory found that 40% of children had a tympanic membrane perforation (TMP) by 18 months of age.3 About 50%–80% of Aboriginal children with CSOM suffer from moderate to severe hearing loss.4,5 This occurs while language and speech are developing and may persist throughout primary school.

There is evidence suggesting that the recommended treatment for ear discharge (twice-daily cleaning and topical ciprofloxacin) can produce cure rates of 70%–90%.6–8 However, a study of Aboriginal children with CSOM in the NT found that less than 30% of children had resolution of ear discharge after 8 weeks of similar treatment.9 This study suggested that ongoing treatment for long periods was difficult for many Aboriginal families living in underresourced and stressful conditions. When children in high-risk communities do not receive appropriate medical treatment for ear disease, using swimming pools to limit levels of ear discharge and possibly reduce bacterial transmission becomes an attractive option.

Traditionally, children with perforated eardrums have been restricted from swimming because of fears of infection. However, it is hypothesised that swimming helps cleanse discharge from the middle ear, nasopharynx and hands and that this benefit may outweigh the risk of introducing infection. Several observational studies have examined the relationship between swimming and levels of skin and ear disease among Aboriginal children.10–14 In a cross-sectional survey, close proximity to a swimming area was associated with reductions of up to 40% in otitis media.10 Two systematic reviews have found that swimming without ear protection does not affect rates of recurrent ear discharge in children with tympanostomy tubes (grommets).15,16 Despite these findings, surveys indicate uncertainty among clinicians regarding water precautions for children with grommets.17–19

Our aim was to conduct a randomised controlled trial (RCT) to better understand the impact of swimming on children with CSOM, and to address a lack of data on ear discharge in older Aboriginal children (aged 5–12 years) with CSOM. We also aimed to obtain microbiological profiles of the nasopharynx and middle ear to help elucidate the cleansing hypothesis.

Methods

Study design

Between August and December 2009, we conducted an RCT examining the impact of 4 weeks of daily swimming in a chlorinated pool on TMPs in Aboriginal children. The Human Research Ethics Committee of the Northern Territory Department of Health and Families and the Menzies School of Health Research approved the study.

Participants and setting

Participants were from two remote Aboriginal communities in the NT. Resident Aboriginal children aged 5–12 years who were found at baseline ear examination to have a TMP were eligible for the trial. Children with a medical condition that prohibited them from swimming were excluded.

Randomisation and blinding

A random sequence stratified by community and age (< 8 years or ≥ 8 years) was generated using Stata version 8 (StataCorp). The allocation sequence was concealed from all investigators. The clinical assessment was performed without knowledge of the group allocation, and laboratory staff were also blinded to group allocation and clinical data.

Intervention

Children in the intervention group swam in a chlorinated pool for 45 minutes, 5 days a week, for 4 weeks. Swimmers did not wear head protection (cap or earplugs) and went underwater frequently. Children in the control group were restricted from swimming for 4 weeks.

Clinical assessments

Participants’ ears were examined in the week before and the week after the intervention using tympanometry, pneumatic otoscopy and digital video otoscopy. Criteria for diagnosis were:

  • Otitis media with effusion: intact and retracted non-bulging tympanic membrane and type B tympanogram

  • Acute otitis media without perforation: any bulging of the tympanic membrane and type B tympanogram

  • Acute otitis media with perforation: middle ear discharge, and perforation present for less than 6 weeks or covering less than 2% of the pars tensa of the tympanic membrane

  • Dry perforation: perforation without any discharge

  • CSOM: perforation (covering > 2% of the pars tensa) and middle ear discharge.

Children with a perforation were examined a second time with a video otoscope. The degree of discharge was graded as nil, scant (discharge visible with otoscope, but limited to middle ear space), moderate (discharge visible with otoscope and present in ear canal), or profuse (discharge visible without otoscope). Drawings of the eardrum and perforations were made, with estimates of the position and size of the perforation as a percentage of the pars tensa. Examiners reviewed the videos in Darwin to confirm the original diagnoses of perforations.

Swab collection and microbiology

Swabs were taken from the nasopharynx and middle ear at both the baseline and final ear examinations. All swabs were cultured on selective media for respiratory bacteria. The bacteria specifically targeted were Streptococcus pneumoniae, non-typeable Haemophilus influenzae, Moraxella catarrhalis and Staphylococcus aureus. Ear discharge swabs were also cultured for Streptococcus pyogenes (Group A Streptococcus), Pseudomonas aeruginosa and Proteus spp.

Swabs stored in skim-milk tryptone glucose glycerol broth20 were thawed and mixed, and 10 μL aliquots were cultured on the following plates: full chocolate agar, 5% horse blood agar containing colistin and nalidixic acid, and chocolate agar with bacitracin, vancomycin, and clindamycin (Oxoid Australia). Ear discharge swabs were also cultured on MacConkey agar plates. Blood plates were incubated at 37°C in 5% CO2, and MacConkey plates at 35°C in air. Bacterial isolates were identified according to standard laboratory procedures.

The density of each of the bacteria on each plate was categorised as: 1) < 20; 2) 20–49; 3) 50–100; 4) > 100 or confluent in the primary inoculum; 5) as for 4, but colonies also in second quadrant of the plate; 6) as for 5, but colonies also in third quadrant; 7) as for 6, but colonies also in fourth quadrant. Dichotomous measures for bacterial load were categorised as low density (< 100 colonies) or high density (≥ 100 colonies).

Outcome measures

Clinical measures

The primary outcome measure was the proportion of children with otoscopic signs of ear discharge in the canal or middle ear space after 4 weeks. Final ear examinations took place 12 hours to 2.5 days after the participants’ last scheduled swim. Prespecified subgroup comparisons were: younger (5–7 years) versus older (8–12 years) children; children who had been prescribed topical antibiotics versus those who had not; degrees of discharge; and smaller (< 25%) versus larger (≥ 25%) perforations.

Microbiological measures

For the nasopharynx, we determined the proportions of children with S. pneumoniae, H. influenzae, M. catarrhalis, any respiratory pathogen (S. pneumoniae, H. influenzae, M. catarrhalis) and S. aureus. For the middle ear, we determined the proportions of children with S. pneumoniae, H. influenzae, M. catarrhalis, S. aureus, Group A Streptococcus, P. aeruginosa and Proteus spp.

Statistical methods and analyses

All participants allocated to a group contributed a clinical outcome for analysis, including children lost to follow-up, whose diagnoses were assumed not to have changed from baseline. Children lost to follow-up were excluded from assessments of microbiological outcomes. Risk differences (RDs) between the study groups were calculated with 95% confidence intervals. The Mann–Whitney U test was used to compare median perforation sizes of the study groups.

Sample size

We hypothesised that 90% of children not swimming would have ear discharge at 28 days and that swimming could reduce this proportion. We specified that a 25% difference between the two groups would be clinically important. Our aim was to recruit a sample of 100 children to provide 80% power to detect a substantial difference of 25% between the two groups.

Results

Parental consent was obtained for 89 eligible children: 41 children in the swimming group and 48 children in the non-swimming group (Box 1). At 4-week follow-up, final ear examinations were conducted on 82 children (36 swimmers and 46 non-swimmers).

At baseline, the study groups were similar in age, sex, perforation size, the presence and degree of ear discharge, and the prevalences of ear diagnoses (Box 2). Although there were no statistically significant differences in the baseline prevalence of bacteria in the nasopharynx or middle ear, swimmers had lower rates of H. influenzae in the nasopharynx and higher rates of S. aureus in both the nasopharynx and middle ear. Of the 89 children, 58 (26 swimmers and 32 non-swimmers) had ear discharge at baseline.

At 4-week follow-up, 56 children had ear discharge: 24 of 41 swimmers compared with 32 of 48 non-swimmers (RD, − 8%; 95% CI, − 28% to 12%). Excluding children lost to follow-up, 21 of 36 swimmers had ear discharge compared with 31 of 46 non-swimmers (RD, − 9%; 95% CI, − 30% to 12%).

Between baseline and 4-week follow-up, there was no statistically significant change in the prevalence of bacteria in the nasopharynx (Box 2). P. aeruginosa infection in the middle ear increased in swimmers, compared with no change in non-swimmers. Non-typeable H. influenzae isolated from ear discharge increased in both groups. Overall, the dominant organisms were S. pneumoniae and H. influenzae in the nasopharynx, and H. influenzae, S. aureus and P. aeruginosa in the middle ear.

Per-protocol analysis of swimmers attending > 75% of swimming classes and non-swimmers adhering to swimming restrictions > 75% of the time indicated that 16 of 24 swimmers had ear discharge at 4-week follow-up, compared with 29 of 44 non-swimmers (RD, 1%; 95% CI, − 23% to 23%).

Rates of discharge were significantly lower in children who were prescribed ciprofloxacin and in children with smaller perforations (Box 3).

Of the 89 children, 65 had no change from their original diagnosis (by child’s worst ear) at 4-week follow-up. Ear discharge failed to resolve in 31 of the 35 participants with moderate to profuse ear discharge at baseline (Box 3). Seven of the 89 children had a perforation that healed (Box 4).

Discussion

We found that regular swimming in a chlorinated pool for 4 weeks did not aid resolution of ear discharge in Aboriginal children with CSOM. At the end of the trial, rates of ear discharge were similar between swimmers and non-swimmers. Our microbiological data also suggest that swimming is unlikely to be effective in removing discharge from the middle ear and nasopharynx, with rates and densities of organisms generally comparable between swimmers and non-swimmers, with little change during the study. Among swimmers, there was an increase in P. aeruginosa middle ear infection, but this was not correlated with new episodes of ear discharge.

Our study is the first RCT to examine the effects of swimming on Aboriginal children with CSOM and also addresses the need for more RCTs examining the impact of swimming on children with grommets. Further, the microbiological data enabled an assessment of the effect of regular swimming on infection in the nasopharynx and middle ear. Other strengths include the blinding of examiners, prespecified subgroup analysis and a follow-up rate of more than 90%.

Our study also has some limitations. We planned to randomly assign 100 children and anticipated that 90% of participants would have ear discharge at follow-up, but we had only 89 participants and 63% with discharge at follow-up, meaning the study was underpowered. Some difficulties were encountered in recruiting children who did not attend school in one community. The possibility of contamination among non-swimmers was also a concern. Parents and school and pool staff assisted in ensuring that non-swimmers did not swim at the pool or at any other water sites, and alternative activities were provided for non-swimmers after school, as this was a popular swimming time. Attendance at swimming and activity classes were monitored, and two portable media players were offered as incentives to children with the highest attendance.

The lack of objective measures for the degree of discharge, perforation size and bacterial density may have contributed to measurement error. It is unlikely that these limitations would prevent a large clinical effect being identified. However, our small sample size means that modest benefits or harms associated with daily swimming may still be possible.

Our results are not consistent with research from two remote communities in Western Australia, which found that rates of TMPs among Aboriginal children halved from about 30% to 15% after swimming pools were installed.11 The potential to improve on our results with longer exposure to swimming is possible. However, the WA study did not follow individual children, and after 5 years the reductions were sustained in only one community.14 Further, the likelihood of significant clinical improvements over a longer period is not supported by our microbiological data. A recent South Australian study also found that the installation of swimming pools in six communities did not affect rates of TMPs among children.12

While swimming may remove some ear and nasal discharge, there is evidence to suggest that cleansing practices alone will not cure CSOM. A Cochrane review of studies conducted in developing countries found that wet irrigation or dry mopping was no more effective than no treatment in resolving ear discharge in children with CSOM (odds ratio, 0.63; 95% CI, 0.36–1.12).21 The review recommended that aural cleansing should be conducted in conjunction with topical antibiotic therapy.21 Future studies could look at the effectiveness of swimming in combination with the application of topical antibiotic therapy.

Over the 4 weeks of our intervention, rates of H. influenzae middle ear infection substantially increased in both swimmers (from 35% to 70%) and non-swimmers (from 50% to 65%). Previous topical antibiotic trials of Aboriginal children (aged 1–16 years) have reported lower baseline rates of H. influenzae in the middle ear, ranging from 5% to 25%.6,9 In contrast, a vaccination trial of Aboriginal infants aged < 24 months found H. influenzae in 85% of new perforations.22 The high levels of H. influenzae ear and nasopharyngeal infection may mean that there is a role for the use of oral antibiotics in combination with topical antibiotics to treat Aboriginal children with CSOM. There may also be benefits from vaccines against H. influenzae in Aboriginal children at high risk of progressing to CSOM.

Simultaneous hand contamination and nasal carriage of S. pneumoniae and H. influenzae is a reliable indicator of TMP in Aboriginal children under 4 years of age.23 Future research could examine rates of hand contamination in relation to swimming, particularly targeting younger children (aged 2–5 years), who are most likely to transmit otitis media bacteria to infants.

In conclusion, it seems unlikely that regular swimming in pools will resolve ear discharge and heal TMPs in the short term. We also found no clear indication that swimming reduces rates of respiratory and opportunistic bacteria in the nasopharynx or middle ear. However, we did not find swimming to be associated with an increased risk of ear discharge. We would not support the practice of restricting children with a TMP from swimming unless it was documented that ear discharge developed directly after swimming (for that particular child). More RCTs are needed to assess more modest (or longer-term) effects of swimming on middle ear disease in Aboriginal children. The combination of swimming and ciprofloxacin treatment may also produce better clinical outcomes and should be investigated.

1 Flowchart of participants through the trial

TMP = tympanic membrane perforation.

2 Participant characteristics at baseline and 4-week follow-up

Baseline

Follow-up

Swimmers
(n = 41)

Non-swimmers (n = 48)

Swimmers
(n = 41)

Non-swimmers (n = 48)

Risk difference
(95% CI)*

Mean age in years (SD)

8.9 (2.4)

8.6 (1.9)

—

—

Male

27 (66%)

31 (65%)

—

—

Ear diagnosis

n = 41 

n = 48

n = 41†

n = 48†

Bilateral closed tympanic membranes

—

—

1/41 (2%)

6/48 (13%)

− 10% (− 23% to 2%)

Unilateral dry TMP

11/41 (27%)

11/48 (23%)

11/41 (27%)

5/48 (10%)

16% (0 to 33%)

Bilateral dry TMPs

4/41 (10%)

5/48 (10%)

5/41 (12%)

5/48 (10%)

2% (− 12% to 17%)

Unilateral wet TMP

12/41 (29%)

13/48 (27%)

10/41 (24%)

12/48 (25%)

− 1% (− 18% to 18%)

Wet TMP and dry TMP

2/41 (5%)

2/48 (4%)

5/41 (12%)

5/48 (10%)

2% (− 12% to 17%)

Bilateral wet TMPs

12/41 (29%)

17/48 (35%)

9/41 (22%)

15/48 (31%)

− 9% (− 27% to 10%)

Median size of TMP as percentage of pars tensa (IQR)

20% (8%–38%)

18% (6%–40%)

15% (4%–32%)

20% (5%–49%)

P = 0.39

Any ear discharge (primary outcome)

26/41 (63%)

32/48 (67%)

24/41 (59%)

32/48 (67%)

− 8% (− 28% to 12%)

Moderate or profuse discharge

16/41 (39%)

19/48 (40%)

20/41 (49%)

25/48 (52%)

− 3% (− 24% to 17%)

Nasopharyngeal bacteria

n = 41 

n = 46‡

n = 35‡

n = 41‡

Streptococcus pneumoniae

28/41 (68%)

33/46 (72%)

19/35 (54%)

27/41 (66%)

− 12% (− 33% to 1%)

Non-typeable Haemophilus influenzae

17/41 (41%)

28/45 (62%)

21/35 (60%)

30/41 (73%)

− 13% (− 34% to 8%)

Moraxella catarrhalis§

17/40 (43%)

17/46 (37%)

6/35 (17%)

14/41 (34%)

− 17% (− 36% to 3%)

Any respiratory pathogen

28/41 (68%)

41/46 (89%)

24/35 (69%)

37/41 (90%)

− 22% (− 40% to − 4%)

Staphylococcus aureus

8/41 (20%)

5/46 (11%)

9/35 (26%)

4/41 (10%)

16% (− 1% to 34%)

At least one high-density respiratory pathogen§

17/35 (49%)

23/43 (53%)

16/35 (46%)

16/41 (39%)

7% (− 15% to 28%)

Middle ear bacteria

n = 24‡

n = 30‡

n = 23‡

n = 32‡

Streptococcus pneumoniae§

1/24 (4%)

4/30 (13%)

0/23

2/32 (6%)

− 6% (− 20% to 9%)

Non-typeable Haemophilus influenzae

8/23 (35%)

14/28 (50%)

16/23 (70%)

20/31 (65%)

5% (− 21% to 29%)

Moraxella catarrhalis§

0/22

0/29

1/21 (5%)

0/31

5% (− 4% to 14%)

Staphylococcus aureus

8/24 (33%)

5/30 (17%)

8/23 (35%)

4/32 (13%)

22% (0 to 45%)

Group A Streptococcus

3/24 (13%)

1/30 (3%)

5/23 (22%)

2/32 (6%)

15% (− 3% to 37%)

Pseudomonas aeruginosa

3/24 (13%)

10/30 (33%)

10/23 (43%)

10/32 (31%)

12% (− 13% to 37%)

Proteus spp.

3/24 (13%)

2/30 (7%)

2/23 (9%)

2/32 (6%)

2% (− 13% to 22%)

TMP = tympanic membrane perforation. IQR = interquartile range. * Unless otherwise indicated. † Includes children lost to follow-up, whose diagnoses were assumed not to have changed from baseline. ‡ Denominators are reduced due to children lost to follow-up, children refusing to have swab taken, or swab being damaged in transportation. § Some plates were contaminated by Proteus spp.

3 Children with ear discharge at final ear examination, by subgroup at baseline

Overall

Swimmers

Non-swimmers

Risk difference (95% CI)

All children with ear discharge at final ear examination

56/89 (63%)

24/41 (59%)

32/48 (67%)

− 8% (− 28% to 12%)

Subgroup

Aged 5–7 years

14/24 (58%)

6/11 (55%)

8/13 (62%)

− 7% (− 44% to 31%)

Aged 8–12 years

42/65 (65%)

18/30 (60%)

24/35 (69%)

− 9% (− 31% to 15%)

Not prescribed topical ciprofloxacin

46/67 (69%)

20/30 (67%)

26/37 (70%)

− 4% (− 26% to 18%)

Prescribed topical ciprofloxacin

10/22 (45%)

4/11 (36%)

6/11 (55%)

− 18% (− 54% to 23%)

Nil discharge

9/31 (29%)

3/15 (20%)

6/16 (38%)

− 18% (− 47% to 15%)

Scant discharge

16/23 (70%)

5/10 (50%)

11/13 (85%)

− 35% (− 66% to 4%)

Moderate or profuse discharge

31/35 (89%)

16/16 (100%)

15/19 (79%)

− 21% (− 1% to 44%)

Small (< 25%) perforation

19/49 (39%)

9/24 (38%)

10/25* (40%)

− 3% (− 29% to 24%)

Large (≥ 25%) perforation

35/38 (92%)

15/17 (88%)

20/21 (95%)

− 7% (− 31% to 13%)

* Perforation size was not estimated for two children in the non-swimming group at baseline.

4 Change in diagnosis (by child’s worst ear) from baseline to final ear examination

Outcome

Overall (n = 89)

Swimmers (n = 41)

Non-swimmers (n = 48)

Dry TMP to closed tympanic membrane

4 (5%)

1 (2%)

3 (6%)

Dry TMP to dry TMP

18 (20%)

11 (27%)

7 (15%)

Dry TMP to wet TMP

9 (10%)

3 (7%)

6 (13%)

Wet TMP to closed tympanic membrane

3 (3%)

0

3 (6%)

Wet TMP to dry TMP

8 (9%)

5 (12%)

3 (6%)

Wet TMP to wet TMP

47 (53%)

21 (51%)

26 (54%)

Improved

15 (17%)

6 (15%)

9 (19%)

Same

65 (73%)

32 (78%)

33 (69%)

Got worse

9 (10%)

3 (7%)

6 (13%)

TMP = tympanic membrane perforation.

Traditional healers help close the gap

IN 2009, THE ROYAL Australian and New Zealand College of Psychiatrists awarded the Mark Sheldon Prize for Indigenous mental health to ngangkari (traditional healers) Andy Tjilari and Rupert Langkatjukur Peter. The two were further honoured in 2011 by the World Council for Psychotherapy with the Sigmund Freud Award (bestowed by the City of Vienna, Austria). The awards recognised their distinguished contributions in mental health to the Aboriginal communities of Central Australia.

Traditional healers of Central Australia celebrates the important work done by these and other ngangkari. It is a rich compilation of stories told by the ngangkari themselves along with artwork and photographs of Central Australia.The tales told by a number of male and female ngangkari reflect their life and cultural experience with respect to their careers as traditional healers within their Aboriginal family and community. The book includes a general discussion of the work of the ngangkari as well as specifics on how they approach topics such as grief, death and dying, substance abuse, mental illness, and the way they work with conventional health services. The services the ngangkari offer to these communities are often conducted in coordination with formal clinical mental health service provision.

This beautiful and insightful work will give the interested reader a window into a cultural experience of healing that is a continuing vital element of the health of the Aboriginal communities in Central Australia. In the ongoing efforts to Closing the Gap, this book is a reminder that solutions to health may be assisted through the wisdom of local people and communities in coordination with the “evidence” that is so prominent in the discussions about health service delivery today.

Changes in smoking intensity among Aboriginal and Torres Strait Islander people, 1994–2008

To the Editor: The recent study by Thomas1 documents the change in smoking intensity of Australian Indigenous people between 1994 and 2008. A significant overall reduction in heavy smoking was observed with a corresponding increase in the proportion of light smoking.

This is an interesting epidemiological observation but it should not be misinterpreted as a public health achievement or as a desirable goal in itself. As Thomas rightly points out, reducing daily cigarette intake is not an effective harm reduction strategy.

Smokers who reduce their daily cigarette intake by more than 50% compensate by having deeper and more frequent puffs to maintain their nicotine levels, thereby neutralising any potential health benefit.2 Even reducing smoking intensity to very low levels (1–4 cigarettes per day) carries substantial risks. Furthermore, there is no evidence to indicate that smoking reduction is associated with a subsequent increase in abstinence rates, unless medication is used.3

The most likely explanations for the reduction in smoking intensity in Indigenous communities are the rising cost of smoking and public health measures, although there are evidence gaps in the research.4 Smoking is still regarded as normal in Indigenous communities and there is scant evidence of a shift in attitudes to smoking.5 Under these circumstances, there is unlikely to be any benefit from reduced daily cigarette consumption in terms of health or abstinence rates.

The goal for clinicians, smokers and communities should always be complete smoking cessation, which has proven, sustained and substantial health benefits.

Changes in smoking intensity among Aboriginal and Torres Strait Islander people, 1994–2008

In reply: Nowhere in my article do I promote reducing the number of cigarettes patients smoke, rather than smoking cessation, as a goal for clinicians. Mendelsohn and Gould have created their own straw man with which to argue.

I explain in the third paragraph of the Discussion that the population changes in smoking intensity may have been caused by previously heavy smokers cutting down (with only modest health benefits) or by younger cohorts never becoming heavy smokers (which will lead to greater health benefits).1 There are early signs of the more important latter change occurring, as has been shown in the United States with more detailed datasets.2

Mendelsohn and Gould are wrong to dismiss these changes as mere epidemiological curiosity. They are a public health achievement, probably caused by the public health measures that I described and which they acknowledge. Together with previously reported trends in smoking behaviour, these changes should lead to lower rates of sickness and early death due to smoking in Aboriginal and Torres Strait Islander people.

Characteristics of the community-level diet of Aboriginal people in remote northern Australia

Dietary improvement for Indigenous Australians is a priority strategy for reducing the health gap between Indigenous and non-Indigenous Australians.1 Poor-quality diet among the Indigenous population is a significant risk factor for three of the major causes of premature death — cardiovascular disease, cancer and type 2 diabetes.2 The 26% of Indigenous Australians living in remote areas experience 40% of the health gap of Indigenous Australians overall.3 Much of this burden of disease is due to extremely poor nutrition throughout life.4

Comprehensive dietary data for Indigenous Australians are not available from national nutrition surveys or any other source. Previous reports on purchased food in remote Aboriginal communities are either dated,5 limited to the primary store5,6 and/or short-term or cross-sectional in design.7,8 These studies have consistently reported low intake of fruit and vegetables, high intake of refined cereals and sugars, excessive sodium intake, and limited availability of several key micronutrients.

The aim of this study was to examine characteristics of the community-level diet in remote communities in the Northern Territory over a 12-month period.

Methods

We examined purchased food in three remote communities in relation to:

  • food expenditure;

  • estimated per capita intake;

  • nutrient profile (macronutrient contribution to energy) and nutrient density (nutrient per 1000 kJ) relative to requirements; and

  • major nutrient sources.

We collected information on community size, remoteness and availability of food in each community as well as community dietary data including all available foods with the exception of traditional foods and foods sourced externally to the community. Alcohol was prohibited in the three study communities at the time of our study.

Monthly electronic food (and non-alcoholic beverage) transaction data were provided by the community-owned store and independent stores in the three communities for July 2010 to June 2011. Food order data were collected from food suppliers for all food services in each of the three communities. All food and beverage items with their accompanying universal product code or store-derived product code, quantity sold, and dollar value (retail price) were imported to a purpose-designed Microsoft Access database9 and linked to the Food Standards Australia New Zealand Australian Food and Nutrient survey specific (AUSNUT 1999 and AUSNUT 200710) and reference (NUTTAB 06) databases (NUTTAB 06 has now been replaced by NUTTAB 2010). Folate dietary equivalent levels per 100 g were modified for bread and flour to equal NUTTAB 2010 levels since mandatory fortification was introduced. Unit weights were derived for all food and drink items and multiplied by the quantity sold to give a total item weight. Food items were categorised into food groups derived from the Australian Food and Nutrient Database AUSNUT 07 food grouping system10 and beverages were further categorised to provide a greater level of detail (Appendix 1). Several nutrient compositions for items not available in these databases were derived from the product’s nutrition information panel, which is mandatory on all packaged foods in Australia, or from standard recipes. Nutrient availability was derived for 21 nutrients. Energy and nutrient content per 100 g edible portion was multiplied by the edible weight (primarily sourced from Australian Food and Nutrient data10) of each of the food and beverage items (adjusted for specific gravity to convert mL to g weight) to derive total energy and nutrient content for each food group.

Completeness of data and accuracy were ensured by: a check on monthly time periods reported, follow-up with providers where a food description or unit weight was not available or where a discrepancy was noted; checking of unit weights against unit dollar value; and a second person checking the matching of foods with nutrient composition data and assigning of food groups.

Data analysis

Data were grouped by community, food source, month and food group and transferred to Stata 10 (StataCorp) for analysis. Data for all food sources were combined (community food supply) and the average monthly and per capita daily weight and dollar value of each food group were calculated. Mean monthly and daily food weights were assumed to approximate mean monthly and daily dietary intakes for the data period.

The populations of each of the three remote communities and the three communities combined were estimated based on the total amount of energy provided through the community-level diet, and, assuming energy balance, were divided by the estimated weighted per capita energy requirement for each of the communities and the three communities combined. The estimated total population was verified against Australian Bureau of Statistics (ABS) estimates.11 The weighted per capita energy requirement was determined for each community using the estimated energy requirement for each age group and sex, as stated in the Nutrient Reference Values for Australia and New Zealand12 (with a physical activity factor of 1.6 [National Health and Medical Research Council — light activity13]) in conjunction with the population age and sex distribution as determined by the 2006 ABS population census for each of these three communities.

Nutrient density was calculated for each nutrient by dividing the total nutrient weight by the energy value of the community food supply. Population-weighted nutrient density requirements were derived using estimated average requirements (EARs).12 The EAR for nutrients is stated as a daily average and varies by age and sex. EARs are estimated to meet the requirements of half the healthy individuals of a particular age group and sex and are used to assess the prevalence of inadequate intakes at a population level.12 A nutrient density level below the weighted EAR per 1000 kJ was considered insufficient in meeting the population’s requirements.

Adequate intake (AI) values were used for nutrients for which no EAR was available (potassium, dietary fibre and vitamin E α-tocopherol equivalents). The midpoint of the AI range for sodium was used. Macronutrient profiles (the proportions of dietary energy from protein, total fat, saturated fat, carbohydrate and total sugar) were compared with acceptable macronutrient distribution ranges.14 Major food sources were defined as foods contributing 10% or more of a specific nutrient.

Ethics approval was provided by the Human Research Ethics Committee of Menzies School of Health Research and the Northern Territory Department of Health and the Central Australian Human Research Ethics Committee. Written informed consent was gained from all participating communities, food businesses and food services.

Results

The estimated total population was 2644. Community populations ranged in estimated size from 163 to 2286 residents of mostly Aboriginal ethnicity and were comparable with regard to age and sex distributions.15 The distance from each community to the nearest food wholesaler ranged from 130 km to 520 km. Variation between the communities in remoteness, size, and number of food outlets is shown in Box 1.

Expenditure patterns

Average per capita monthly spending on food and non-alcoholic beverages in communities A, B and C, respectively, was $394 (SD, $31), $418 (SD, $82) and $379 (SD, $80). About one-quarter of all money spent on food and beverages was on beverages (combined communities, 24.8%; SD, 1.4%), with soft drinks contributing 11.6%–16.1% to sales across the three communities (combined communities, 15.6%; SD 1.2%) (Appendix 2). This compares to less than 10% in total spent on fruit and vegetables in each of the three communities (7.3%, 9.1% and 8.9%; combined communities, 2.2% [SD, 0.2%] on fruit and 5.4% [SD, 0.4%] on vegetables) (Appendix 2).

Per capita daily intake

Based on population estimates, there appeared to be differences in the daily per capita volume of many food groups between community A compared with communities B and C and less notable differences between communities B and C (Appendix 3).

On average, per capita daily intake of beverages (including purchased water and liquid tea) was 1464 g (SD, 130.5 g) with sugar-sweetened soft drinks comprising 298–497 g across communities (Appendix 3). Liquid tea constituted most of the remaining beverage volume. Daily per capita fruit and vegetable intake in community A (122 g) was just over half that of communities B (222 g) and C (247 g) (Appendix 3).

Macronutrient profile

For community A, the proportion of dietary energy as carbohydrate was at the higher end of the recommended range; for communities B and C it was within the recommended range. Sugars contributed 25.7%–34.3% of the total proportion of dietary energy across the three communities (Box 2), 71% of which was table sugar and sugar-sweetened beverages. The proportion of dietary energy from fat was within the acceptable range for each community, and lower in community A compared with communities B and C. The proportion of dietary energy as saturated fat was within the recommended range for community A and higher than recommended for communities B and C. The proportion of dietary energy as protein was lower than the recommended minimum in all three communities (Box 2).

Micronutrient density

With reference to weighted EARs (or AIs) per 1000 kJ and nutrients measured, in all three communities the diet was insufficient in calcium, magnesium, potassium and fibre (Box 3). Iron, vitamin C and folate equivalents were all around double the weighted EAR per 1000 kJ and niacin equivalents were nearly four times the EAR (Box 3). Sodium was the nutrient provided in the greatest excess, at nearly six times the midpoint of the average intake range (Box 3). Most nutrient density values appeared lower in community A compared with communities B and C (Appendix 4).

Major nutrient sources

In all three communities, white bread fortified with fibre and a range of micronutrients was a major source of protein, fibre, iron, sodium, calcium, dietary folate, potassium, magnesium and B-group vitamins (Appendix 5). Sugar and sugar-sweetened beverages provided 65%–72% of total sugars (Appendix 5). Bread, salt and baking powder were major sources of sodium in all three communities. Major food sources of all nutrients were similar across the three communities (Appendix 5).

Discussion

Our comprehensive assessment of the community diet averaged over a 12-month period showed a high intake of refined cereals and added sugars, low levels of fruit, vegetables and protein, limiting key micronutrients, and excessive sodium intake. Our findings confirm recent and past reports of dietary quality in remote Aboriginal communities.5,8 We report food expenditure and dietary patterns that are similar to those reported previously using store sales data alone,5,6,8 as are the limiting nutrients (protein, potassium, magnesium, calcium and fibre).8

A striking finding from our study is the high expenditure on beverages and corresponding high intake of sugar-sweetened beverages coupled with low expenditure (and low intakes) of fruit and vegetables.

The level of sugar-sweetened soft drinks reported for communities B and C is in line with what we have previously reported for 10 NT communities from store data alone.6 The apparently substantially higher per capita volume reported for community A warrants further investigation, which could include examining variation in regional consumption, food delivery systems and food outlets. Similarly high per capita consumption of sugar-sweetened beverages has been reported among Aboriginal and Torres Strait Islander children in regional New South Wales (boys, 457 g/day; girls, 431 g/day) and for children at the national level (364.7 g/day).18,19 The high volume of tea purchased is also of concern, as tea is generally consumed as a sugar-sweetened beverage.

The low daily fruit and vegetable intake reported for the three study communities (which on average equated to 0.3 to 0.7 serves of fruit and 1.1 to 2.1 serves of vegetables) is in range with the reported average of 0.4 serves of fruit and 0.9 serves of vegetables per person per day sold through 10 NT community stores in 2009,6 but lower than intakes self-reported among other Aboriginal populations in remote Queensland and regional NSW.18,20,21 Our estimates do suggest improved intakes compared with the low levels of fruit and vegetable intake reported nearly three decades earlier for six remote NT communities.5 Caution needs to be applied in making comparisons with past studies owing to use of different methodologies. It has been estimated that increasing fruit and vegetable consumption to up to 600 g per day could reduce the global burden of ischaemic heart disease and stroke by 31% and 19%, respectively.22 The benefits for the Indigenous population are likely to be much greater, considering their currently low intake of fruit and vegetables and high burden of disease.

A further disturbing aspect of the diet is that fibre-modified and fortified white bread is providing a large proportion of key nutrients, including protein, folate, iron, calcium and magnesium, and unacceptably high levels of sodium. Similarly, among Aboriginal and Torres Strait Islander children in regional NSW, bread was also reported to be a major dietary source of energy, salt and fibre.18 It is alarming that white bread is providing a large percentage of dietary protein when it is a poor protein source. Considering the high-quality protein foods traditionally consumed by Aboriginal Australians,23 this apparent shift to a low-protein and high-carbohydrate diet needs investigation. Traditional foods, such as fish and other seafood, eggs and meat provide high-quality protein, but are unlikely to be significant at the population level if not accessed frequently and by a substantial proportion of the population.

The extremely high rates of preventable chronic disease experienced among Aboriginal people in remote Australia and the high intake of sugar-sweetened beverages, unacceptably low levels of fruit and vegetables, and limiting essential nutrients, provide a compelling rationale that more needs to be done to improve diet and nutrition. Poverty is a key driver of food choice24–26 and although most Indigenous people living in remote communities are in the low income bracket, a standard basket of food costs, on average, 45% more in remote NT communities than in the NT capital.27 People in the study communities spend more on food ($379 to $418 per person per month) compared with the expenditure estimated for other Australians ($314 per person per month with 2.6 persons per household).28 Our study provides the only available estimate of remote community food and drink expenditure that we know of. Household expenditure data are not available for very remote Australia, representing a gap in information on food affordability, a major determinant of health.

Our study highlighted some important differences in dietary quality between the study communities, with the dietary profile for community A being generally poorer. This may be indicative of intercommunity or regional differences, such as community size, number of food outlets, location and remoteness, access to food outlets, level of subsistence procurement and use of traditional foods, climate, housing or water quality, and warrants broader investigation.

As with individual-level dietary assessment, there are limitations in estimating community-level dietary intake. An inherent issue in community-level per capita measures in research is the difficulty of determining the population for the study period, so caution is required in using the values presented here; however, the total population (2644) was verified against ABS predicted estimates for the 2011 Australian remote Indigenous population (2638) and was within 4% of the later released ABS census data collected in 2010 for the three study communities (2535). Further, monthly per capita dietary intake estimations were averaged over a 12-month period and are likely to take into account the fluctuations in population that occur in remote communities seasonally and over time. A strength of our study is that expenditure patterns based on proportional spending, macronutrient profile and nutrient density provide an assessment of dietary quality that are entirely independent of population size estimates. Furthermore, as dietary data are derived from food sales records rather than self-reported data, they provide an objective assessment of diet quality. Limitations in using food sales data as a measure of dietary intake have been reported previously.8 Estimated per capita energy intakes for communities A and B differed by less than 10% from per capita requirements derived from 2010 ABS census population figures, indicating completeness in food sale data. Estimated energy intakes for community C were lower than required but 81% of per capita requirements.

Reports on dietary quality are also limited by the accuracy of food composition databases. For example, the range of nutrients presented for each food in the Australian food composition database varies depending on the analytical data available. Nutrient levels reported in this study are based on currently available nutrient composition data.29

A limitation in assessing the nutritional quality of the community-level diet using purchased food data is the exclusion of traditional food intake. It is assumed that traditional food contributes minimally to community-level dietary intake, as not all families have access to traditional foods and procurement usually does not occur on a regular basis. However, the contribution of traditional food to dietary intake has not been investigated. We recognise it would be important in future studies to quantify the contribution of traditional foods to total food intake. The low expenditure on (and therefore low intake of) high-quality protein foods suggests that either these foods are not affordable, or that possibly these foods are accessed through subsistence procurement. However, mean daily energy intake estimates based on 2010 census data indicate that the great majority of energy required is provided through the imported food supply.

Despite these limitations, this study provides an objective, contemporary and comprehensive assessment of the community-level diet in three remote Indigenous communities without the inherent limitations of individual-level dietary intake assessment. It provides evidence on key areas of concern for dietary improvement in remote Aboriginal communities.

Very poor dietary quality has continued to be a characteristic of community nutrition profiles in remote Indigenous communities in Australia for at least three decades. Significant proportions of a number of key micronutrients are provided as fortification in a diet derived predominantly from otherwise poor-quality, highly processed foods. Ongoing monitoring (through use of food sales data) of community-level diet is needed to better inform community and wider level policy and strategy development and implementation. Low income is undoubtedly a key driver of diet quality. Further evidence regarding the impact of the cost of food on food purchasing in this context is urgently needed and the long-term cost benefit of dietary improvement needs to be considered.

1 Community characteristics

Population, and age and/or
sex distribution*

Community

2006

2010

Estimated population†

Distance from food wholesaler; location‡

Access

Food stores

Food services

A

1697 
(49% male;
703 residents < 18 yrs)

2124 
(50% male)

2286

> 500 km; island in Top End region

Regular daily flight

Community-owned store. Two independent stores

Aged care meals, child care, school canteen, school lunch program, breakfast program

B

250 
(49% male;
94 residents <18 yrs)

210 
(49% male)

202

> 400 km; central desert region

Sealed and unsealed road

Community-owned store

Aged care meals,
school lunch program,
child care

C

217 
(43% male;
73 residents <18 yrs)

201 
(49% male)

163

< 150 km; central desert region

Sealed and unsealed road

Community-owned store

Aged care meals, child care,
school lunch program,
breakfast program

* Based on Australian Bureau of Statistics (ABS) census data.11,15 † 2644 was derived for the total study population based on the total energy available in the purchased food supply
and the weighted per capita energy requirement based on the total population age and sex distribution. This population size was used for analyses where data for all communities were combined rather than the total of 2651. ‡ All three communities are classified by the ABS Australian Standard Geographical Classification (http://www.health.gov.au/internet/otd/publishing.nsf/Content/locator) as RA5 (very remote). ◆

2 Estimated energy availability and macronutrient profile, overall and by community

Energy intake

Community A

Community B

Community C

All communities

Estimated per capita energy intake based on 2010 census population (kJ)

9845

9119

7623

9608

Estimated per capita energy intake, based on estimated energy requirement* (kJ [SD])

9147 (927)

9480 (1644)

9400 (1740)

9212 (856)

Macronutrient distribution as a proportion of dietary energy (% [SD])

Recommended range14

Protein

12.5% (0.3)

14.1% (0.8)

13.4% (0.6)

12.7% (0.3)

15%–25%

Fat

24.5% (0.6)

31.6% (1.5)

33.5% (1.1)

25.7% (0.6)

20%–35%

Saturated fat

9.4% (0.3)

11.6% (0.6)

12.1% (0.3)

9.7% (0.3)

< 10%

Carbohydrate

62.1% (0.8)

53.3% (1.8)

52.1% (1.1)

60.7% (0.8)

45%–65%

Sugars

34.3% (0.8)

28.9% (2.2)

25.7% (1.8)

33.4% (0.7)

< 10%†

* Estimated energy requirements were calculated by age group (1–3 years; 4–8 years; 9–13 years; 14–18 years; 19–30 years; 31–50 years; 51–70 years; > 70 years) and sex based on Nutrient Reference Values for Australia and New Zealand, tables 1–3.11 For age 19 to > 70 years, the midpoint height and weight of each adult age group was used. For < 18 years, the midpoint of the estimated energy requirement range across each age and sex category was used. Energy expenditure was estimated at 1.6 basal metabolic rate overall. We estimated 8% of women aged 14–50 years were pregnant and 8% were breastfeeding, based on Australian Bureau of Statistics 2006 births data, table 9.216 and 2006 census data for women aged 13–54 years.15 † Recommendation for ‘‘free sugars’’ — all monosaccharides and disaccharides added to foods by the manufacturer, cook or consumer, plus sugars naturally present in honey, syrups and fruit juices.17  ◆

3 Nutrient per 1000 kJ as a percentage of weighted estimated average requirement (EAR) per 1000 kJ,* overall and by community

* Adequate intake values were used for nutrients for which no EAR was available (potassium, dietary fibre, vitamin E α-tocopherol equivalents, sodium).