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.

A time and a place

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Beyond cultural security; towards sanctuary

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

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

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

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

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

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

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.

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

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

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

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).