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Background and ObjectivePrenatal alcohol exposure is a common preventable cause of intellectual disability, but alcohol useremains high during pregnancy. We identified where Australian women obtained information about alcohol during pregnancy, their preferred sources of information, and their perceptions of the role of health professionals in providing information. Materials and MethodsIn 2006, 1103 nonpregnant Australian women of childbearing age (18–45 years) were interviewed using computer-assisted telephone interview. Information about their actual and preferred sources of information about consuming alcohol during pregnancy and the perceived role of health professionals in pregnancy education were obtained.ResultsMost (99%) of the Australian women interviewed said information about the effects of consuming alcohol during pregnancy should be readily available, but only half had sighted any such information. Brochures were the most-sighted source (16%), followed by media programs/articles (13%). Women preferred health professionals (52%) as the best source of information, followed by television advertisements (12%). Health professional platforms (e.g., antenatal classes) were preferred by women who had previously given birth, while the Internet was preferred by nulliparous and Australian-born women. Message recall was associated with knowledge that alcohol consumption during pregnancy can cause fetal alcohol spectrum disorder, growth problems, and lifelong disabilities in a child (P < 0.05). Women agreed that health professionals should ask pregnant women about alcohol, advise how much alcohol consumption is safe during pregnancy, and advise pregnant women or those planning pregnancy to give up alcohol consumption.

Whole exome sequencing (WES) is a popular and successful technology which is widely used in both research and clinical settings. However, there is a paucity of reference data for Aboriginal Australians to underpin the translation of health-based genomic research. Here we provide a catalogue of variants called after sequencing the exomes of 50 Aboriginal individuals from the Northern Territory (NT) of Australia and compare these to 72 previously published exomes from a Western Australian (WA) population of Martu origin. Sequence data for both NT and WA samples were processed using an ‘intersect-then-combine’ (ITC) approach, using GATK and SAMtools to call variants. A total of 289,829 variants were identified in at least one individual in the NT cohort and 248,374 variants in at least one individual in the WA cohort. Of these, 166,719 variants were present in both cohorts, whilst 123,110 variants were private to the NT cohort and 81,655 were private to the WA cohort. Our data set provides a useful reference point for genomic studies on Aboriginal Australians., Measurement(s)Aboriginal Australian • DNA • sequence feature annotationTechnology Type(s)Whole Exome Sequencing • DNA sequencing • sequence annotationFactor Type(s)ancestry • sex • ageSample Characteristic - OrganismHomo sapiensSample Characteristic - LocationNorthern Territory Machine-accessible metadata file describing the reported data: 10.6084/m9.figshare.12040638

Historically, neural tube defects (NTD) in Australia affected around 1 in every 1000 births; 42% higher for Aboriginal births. Following firm evidence of the protective effect of periconceptional folate, health promotion activities encouraged increased folate intake through diet and supplements and limited voluntary food fortification. A 30% reduction in NTD was observed in non-Aboriginal but not Aboriginal infants, widening the disparity between Aboriginal and non-Aboriginal rates. Mandatory flour fortification with folic acid in 2009, led to further reductions in overall NTD, and greater reduction among Aboriginal infants, such that rates in Aboriginal and non-Aboriginal infants were similar by 2010–2014. Elimination of this disparity will make a small but important contribution to the Australian government's Closing the Gap initiative to reduce disadvantage among Aboriginal people. Long-term, complete, high-quality surveillance data on NTD have been of great value in monitoring trends in and evaluation of public health interventions for NTD in Australia.

Ten years have passed since the release of the final report of the World Health Organization (WHO) Commission on Social Determinants of Health (CSDH),1 a landmark document that provided a global blue-print for the health promotion community and the stakeholders we work with. Three overarching recommendations were outlined, improving daily living conditions; tackling the in equitable distribution of power, money and resources; and measuring and understanding the problem and assessing the impact of action.1 The extent to which progress has been, and continues to be, made is contested. This editorial briefly reflects on what has been achieved over the past decade —in broad terms—about action on the social determinants of health (SDH) in Australia. We deliberately take a balanced view by highlighting the weaknesses and strengths in what has been achieved by governments, non-government organisations,research institutions, peak bodies and civil society. We also reflection the ongoing role that the Australian Health Promotion Association (AHPA) has played in advancing our understanding about, and action on, the SDH.

Background Rheumatic heart disease (RHD) after group A streptococcus (GAS) infections is heritable and prevalent in Indigenous populations. Molecular mimicry between human and GAS proteins triggers proinflammatory cardiac valve-reactive T cells. Methods Genome-wide genetic analysis was undertaken in 1263 Aboriginal Australians (398 RHD cases; 865 controls). Single-nucleotide polymorphisms were genotyped using Illumina HumanCoreExome BeadChips. Direct typing and imputation was used to fine-map the human leukocyte antigen (HLA) region. Epitope binding affinities were mapped for human cross-reactive GAS proteins, including M5 and M6. Results The strongest genetic association was intronic to HLA-DQA1 (rs9272622; P = 1.86 × 10-7). Conditional analyses showed rs9272622 and/or DQA1*AA16 account for the HLA signal. HLA-DQA1*0101_DQB1*0503 (odds ratio [OR], 1.44; 95% confidence interval [CI], 1.09-1.90; P = 9.56 × 10-3) and HLA-DQA1*0103_DQB1*0601 (OR, 1.27; 95% CI, 1.07-1.52; P = 7.15 × 10-3) were risk haplotypes; HLA_DQA1*0301-DQB1*0402 (OR 0.30, 95%CI 0.14-0.65, P = 2.36 × 10-3) was protective. Human myosin cross-reactive N-terminal and B repeat epitopes of GAS M5/M6 bind with higher affinity to DQA1/DQB1 alpha/beta dimers for the 2-risk haplotypes than the protective haplotype. Conclusions Variation at HLA_DQA1-DQB1 is the major genetic risk factor for RHD in Aboriginal Australians studied here. Cross-reactive epitopes bind with higher affinity to alpha/beta dimers formed by risk haplotypes, supporting molecular mimicry as the key mechanism of RHD pathogenesis.

IntroductionPregnant women and infants are at risk of severe influenza and pertussis infection. Inactivated influenza vaccine (IIV) and diphtheria-tetanus-acellular pertussis vaccine (dTpa) are recommended during pregnancy to protect both mothers and infants. In Australia, uptake is not routinely monitored but coverage appears sub-optimal. Evidence on the safety of combined antenatal IIV and dTpa is fragmented or deficient, and there remain knowledge gaps of population-level vaccine effectiveness. We aim to establish a large, population-based, multi-jurisdictional cohort of mother-infant pairs to measure the uptake, safety and effectiveness of antenatal IIV and dTpa vaccines in three Australian jurisdictions. This is a first step toward assessing the impact of antenatal vaccination programmes in Australia, which can then inform government policy with respect to future strategies in national vaccination programmes.Methods and analysis‘Links2HealthierBubs’ is an observational, population-based, retrospective cohort study established through probabilistic record linkage of administrative health data. The cohort includes births between 2012 and 2017 (~607 605 mother-infant pairs) in jurisdictions with population-level antenatal vaccination and health outcome data (Western Australia, Queensland and the Northern Territory). Perinatal data will be the reference frame to identify the cohort. Jurisdictional vaccination registers will identify antenatal vaccination status and the gestational timing of vaccination. Information on maternal, fetal and child health outcomes will be obtained from hospitalisation and emergency department records, notifiable diseases databases, developmental anomalies databases, birth and mortality registers.Ethics and disseminationEthical approval was obtained from the Western Australian Department of Health, Curtin University, the Menzies School of Health Research, the Royal Brisbane and Women’s Hospital, and the West Australian Aboriginal Health Ethics Committees. Research findings will be disseminated in peer-reviewed journals, at scientific meetings, and may be incorporated into communication materials for public health agencies and the public.

In common with colonized Indigenous people worldwide, many Australian Aboriginal people experience inequitable health outcomes. While the commitment and advocacy of researchers and health practitioners has resulted in many notable improvements in policy and practice, systemic and structural impediments continue to restrain widespread gains in addressing Indigenous health injustices. We take Rheumatic Heart Disease (RHD), a potent marker of extreme health inequity, as a case study, and critically examine RHD practitioners' perspectives regarding the factors that need to be addressed to improve RHD prevention and care. This study is an important explanatory component of a broader study to inform new clinical practices, and health system strategies and policies to reduce RHD. A decolonising, critical medical anthropology (CMA) analysis of findings from 22 RHD practitioner in-depth interviews conducted in May 2016 revealed both practitioners' perceptions of health system shortcomings and a sense of hopelessness and powerlessness to transform existing health system inequities, the negative impacts of which were subsequently confirmed in a separate study of RHD patients' lived realities. We reveal how biomedical dominance, normalized deficit discourses and systemic racism influence the current policy and practice landscape, narrowing the intercultural space for productive dialogue and reinforcing the conditions that cause disease. To counter biomedical approaches that contribute to existing health inequities in health care, we recommend localized, strength-based, community-led research projects focused on actions that use critical decolonizing social science approaches to achieve system change. We demonstrate the importance of integrating biological and social sciences approaches in research, education/training, and practice to: 1) be guided by Indigenous strengths, knowledges and worldview, and 2) adopt a critical reflexive stance to examine systems, structures and practices. Such an approach facilitates productive cross-cultural dialogue and social transformation; providing direction and hope to practitioners, enhancing their knowledge, skills and capacity and improving Aboriginal health outcomes.

Can equitable health outcomes across Australia be provided by increasingly urban-dominated populations? The Australian HOT North (Improving Health Outcomes in the Tropical North) program has tackled the increasing urban-rural/remote health divide by focusing on three components of the health research ecosystem – researcher retention and recruitment, researcher-practitioner collaborations, and knowledge transfer by forming cross-jurisdictional and multi-disciplinary networks and delivering on-country knowledge translation. We propose that a more widespread implementation of locally-designed research and practice, embedded alongside programs that strengthen cross-jurisdictional networks, would increase health equity in rural and remote areas.

Background The consent and community engagement process for research with Indigenous communities is rarely evaluated. Research protocols are not always collaborative, inclusive or culturally respectful. If participants do not trust or understand the research, selection bias may occur in recruitment, affecting study results potentially denying participants the opportunity to provide more knowledge and greater understanding about their community. Poorly informed consent can also harm the individual participant and the community as a whole. Methods Invited by local Aboriginal community leaders of the Fitzroy Valley, the Kimberley, Western Australia, The Picture Talk project explores the consent process for research. Focus groups of Aboriginal community members were conducted to establish preferences for methods of seeking individual consent. Transcripts were analysed through NVivo10 Qualitative software using grounded theory with inductive and deductive coding. Themes were synthesised with quotes highlighted. Results Focus groups with Aboriginal community members (n = 6 focus groups of 3–7 participants) were facilitated by a Community Navigator as a cultural guide and interpreter and a researcher. Participants were recruited from all main language groups of the Fitzroy Valley – Gooniyandi, Walmajarri, Wangkatjungka, Bunuba and Nikinya. Participants were aged ≥18 years, with 5 female groups and one male group. Themes identified include: Reputation and trust is essential; The Community Navigator is key; Pictures give the words meaning – milli milli versus Pictures; Achieving consensus in circles; Signing for consent; and Research is needed in the Valley. Conclusion Aboriginal communities of the Fitzroy Valley recommend that researchers collaborate with local leaders, develop trust and foster a good reputation in the community prior to research. Local Aboriginal researchers should be employed to provide cultural guidance throughout the research process and interpret local languages especially for elders. Pictures are preferred to written text to explain research information and most prefer to sign for consent. The Fitzroy Valley welcomes research when collaborative and for the benefit of the community. Future research could include exploring how to support young people, promote health screening and improve understanding of medical knowledge.

Aim To compare proportions of live births subsequently described as having cerebral palsy (CP), the distributions of associated impairments, and the causes of postneonatal CP between Aboriginal and Torres Strait Islander (Indigenous) and non-Indigenous populations in Australia. Method Data from statutory birth records and CP registers for the 1996 to 2005 birth cohort in Queensland, Western Australia, and the Northern Territory were stratified by Indigenous status and whether the CP was acquired pre/perinatally or postneonatally. Relative risks associated with Indigenous status were estimated and the distributions of causes of postneonatal CP compared. Results Indigenous births had a relative risk of 4.9 (95% confidence interval [CI] 3.0–7.9) for postneonatal CP but only of 1.42 (95% CI 1.2–1.7) for pre/perinatal CP. Almost half of postneonatal CP in Indigenous infants resulted from infection, whereas for non-Indigenous infants the most frequent cause was cerebrovascular accident. The impairments of Indigenous CP and of postneonatally acquired CP tended to be more numerous and more severe. Interpretation Indigenous children are at significantly greater risk of CP, particularly postneonatal CP. The predominant cause of postneonatal CP in non-Indigenous children has shifted to cerebrovascular accident over time; however, infections followed by head injury are still the most frequent causes in Indigenous infants.

IntroductionResearch with Indigenous populations is not always designed with cultural sensitivity. Few publications evaluate or describe in detail seeking consent for research with Indigenous participants. When potential participants are not engaged in a culturally respectful manner, participation rates and research quality can be adversely affected. It is unethical to proceed with research without truly informed consent.Methods and analysisWe describe a culturally appropriate research protocol that is invited by Aboriginal communities of the Fitzroy Valley in Western Australia. The Picture Talk Project is a research partnership with local Aboriginal leaders who are also chief investigators. We will interview Aboriginal leaders about research, community engagement and the consent process and hold focus groups with Aboriginal community members about individual consent. Cultural protocols will be applied to recruit and conduct research with participants. Transcripts will be analysed using NVivo10 qualitative software and themes synthesised to highlight the key issues raised by the community about the research process. This protocol will guide future research with the Aboriginal communities of the Fitzroy Valley and may inform the approach to research with other Indigenous communities of Australia or the world. It must be noted that no community is the same and all research requires local consultation and input. To conduct culturally sensitive research, respected local people from the community who have knowledge of cultural protocol and language are engaged to guide each step of the research process from the project design to the delivery of results.Ethics and disseminationEthics approval was granted by the University of Sydney Human Research Ethics Committee (No. 2012/348, reference:14760), the Western Australia Country Health Service Ethics Committee (No. 2012:15), the Western Australian Aboriginal Health Ethics Committee and reviewed by the Kimberley Aboriginal Health Planning Forum Research Sub-Committee (No. 2012–008). Results will be disseminated through peer review articles, a local Fitzroy Valley report and conference presentations.

BackgroundRheumatic heart disease (RHD) following Group A Streptococcus (GAS) infections is heritable and prevalent in Indigenous populations. Molecular mimicry between human and GAS proteins triggers pro-inflammatory cardiac valve-reactive T-cells.MethodsGenome-wide genetic analysis was undertaken in 1263 Aboriginal Australians (398 RHD cases; 865 controls). Single nucleotide polymorphisms (SNPs) were genotyped using Illumina HumanCoreExome BeadChips. Direct typing and imputation was used to fine-map the human leukocyte antigen (HLA) region. Epitope binding affinities were mapped for human cross-reactive GAS proteins, including M5 and M6.ResultsThe strongest genetic association was intronic to HLA-DQA1 (rs9272622; P=1.86x10−7). Conditional analyses showed rs9272622 and/or DQA1*AA16 account for the HLA signal. HLA-DQA1*0101_DQB1*0503 (OR 1.44, 95%CI 1.09-1.90, P=9.56x10−3) and HLA-DQA1*0103_DQB1*0601 (OR 1.27, 95%CI 1.07-1.52, P=7.15x10−3) were risk haplotypes; HLA_DQA1*0301-DQB1*0402 (OR 0.30, 95%CI 0.14-0.65, P=2.36x10−3) was protective. Human myosin cross-reactive N-terminal and B repeat epitopes of GAS M5/M6 bind with higher affinity to DQA1/DQB1 alpha/beta dimers for the two risk haplotypes than the protective haplotype.ConclusionsVariation at HLA_DQA1-DQB1 is the major genetic risk factor for RHD in Aboriginal Australians studied here. Cross-reactive epitopes bind with higher affinity to alpha/beta dimers formed by risk haplotypes, supporting molecular mimicry as the key mechanism of RHD pathogenesis.

Background Researchers are required to seek consent from Indigenous communities prior to conducting research but there is inadequate information about how Indigenous people understand and become fully engaged with this consent process. Few studies evaluate the preference or understanding of the consent process for research with Indigenous populations. Lack of informed consent can impact on research findings. Methods The Picture Talk Project was initiated with senior Aboriginal leaders of the Fitzroy Valley community situated in the far north of Western Australia. Aboriginal people were interviewed about their understanding and experiences of research and consent processes. Transcripts were analysed using NVivo10 software with an integrated method of inductive and deductive coding and based in grounded theory. Local Aboriginal interpreters validated coding. Major themes were defined and supporting quotes sourced. Results Interviews with Aboriginal leaders (n = 20) were facilitated by a local Aboriginal Community Navigator who could interpret if necessary and provide cultural guidance. Participants were from all four major local language groups of the Fitzroy Valley; aged 31 years and above; and half were male. Themes emerging from these discussions included Research—finding knowledge; Being respectful of Aboriginal people, Working on country, and Being flexible with time; Working together with good communication; Reciprocity—two-way learning; and Reaching consent. Conclusion The project revealed how much more there is to be learned about how research with remote Aboriginal communities should be conducted such that it is both culturally respectful and, importantly, meaningful for participants. We identify important elements in community consultation about research and seeking consent. Electronic supplementary material The online version of this article (doi:10.1186/s12910-017-0191-z) contains supplementary material, which is available to authorized users.

BACKGROUND: Improvements in the rate of infant mortality (death in first year of life) have not occurred in recent years. This study investigates the association between maternal alcohol-use disorder and sudden infant death syndrome (SIDS) and infant mortality not classified as SIDS using linked, population-based health and mortality data. METHODS: Exposed mothers were identified through the presence of an International Classification of Diseases 9/10 alcohol diagnosis, a proxy for alcohol-use disorder, recorded on health, mental health, and/or drug and alcohol datasets (1983–2005). Comparison mothers without an alcohol diagnosis were frequency matched to exposed mothers on maternal age within maternal race and year of birth of their children. All offspring with their birth recorded on the Midwives Notification System compose the exposed (n = 21 841) and comparison (n = 56 054) cohorts. Cases of SIDS (n = 303) and infant mortality excluding SIDS (n = 598) were identified through linkage with the Western Australian Mortality Register. Analyses were conducted by using Cox regression and results presented as adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs). RESULTS: The highest risk of SIDS occurred when a maternal alcohol diagnosis was recorded during pregnancy (aHR 6.92, 95% CI 4.02–11.90) or within 1 year postpregnancy (aHR 8.61, 95% CI 5.04–14.69). An alcohol diagnosis recorded during pregnancy more than doubled the risk of infant deaths (excluding SIDS) (aHR 2.35, 95% CI 1.45–3.83). Maternal alcohol-use disorder is attributable for at least 16.41% (95% CI 9.73%–23.69%) of SIDS and 3.40% (95% CI 2.28%–4.67%) of infant deaths not classified as SIDS. CONCLUSIONS: Maternal alcohol-use disorder is a significant risk factor for SIDS and infant mortality excluding SIDS.

Aim The aim of this study was to examine the association between maternal alcohol use disorder and intellectual disability in children. Method All mothers with an International Classification of Diseases (ICD) 9 and/or 10 alcohol-related diagnosis, a proxy for alcohol use disorder, recorded on the Western Australian health, mental health, and drug and alcohol data sets were identified through the Western Australian Data Linkage Unit (n=5614 non-Aboriginal; n=2912 Aboriginal). A comparison cohort of mothers without an alcohol-related diagnosis was frequency matched on maternal age within maternal Aboriginal status and year of birth of their children. Linkage with the Western Australian Midwives Notification System (1983–2001) identified all births to these mothers (n=10 664 and 7907 respectively). Linkage to the Western Australian Intellectual Disability Database and Register of Developmental Anomalies identified cases of intellectual disability with no identified genetic origin (intellectual disability) (n=1487) and fetal alcohol syndrome (n=66). Odds ratios (ORs) and 95% confidence intervals (CIs) for intellectual disability were calculated using logistic regression incorporating generalized estimating equations and used to estimate population-attributable fractions. Results At least 3.8% (95% CI 2.84–4.89%) of cases of intellectual disability could be avoided by preventing maternal alcohol use disorder: 1.3% (95% CI 0.81–1.86%) in non-Aboriginal and 15.6% (95% CI 10.85–20.94%) in Aboriginal children. We observed a three-fold increase in the adjusted odds of intellectual disability in children of mothers with an alcohol-related diagnosis recorded during pregnancy (non-Aboriginal OR 2.89, 95% CI 1.62–5.18; Aboriginal OR 3.12, 95% CI 2.13–4.56), with a net excess proportion of 3.7% and 5.5% respectively. One-third (32%) of children diagnosed with fetal alcohol syndrome had intellectual disability. Interpretation Maternal alcohol use disorder is the leading known risk factor for intellectual disability with no identified genetic origin.

Please cite this paper as: O’Leary C, Jacoby P, D’Antoine H, Bartu A, Bower C. Heavy prenatal alcohol exposure and increased risk of stillbirth. BJOG 2012;119:945–952. Objective To investigate the association between heavy prenatal alcohol exposure and stillbirth. Design Data linkage cohort study. Setting Western Australia (WA). Population The exposed cohort included mothers with an alcohol-related diagnosis (International Classification of Diseases, ninth/tenth revisions) recorded in health data sets and all their offspring born in WA (1983–2007). Mothers without an alcohol-related diagnosis and their offspring comprised the comparison cohort. Methods Exposed and comparison mothers were identified through the WA Data Linkage System. Odds ratios for stillbirth at 20 + weeks of gestation were estimated by logistic regression, stratified by Aboriginal status. Main outcome measures The proportion of stillbirths at 20 + weeks of gestation is presented per 1000 births, as well as adjusted odds ratios (aOR) and 95% confidence intervals (95% CI), and population-attributable fractions. Results Increased odds of stillbirth were observed for mothers with an alcohol-related diagnosis at any stage of their life for both non-Aboriginal (aOR 1.36; 95% CI 1.05–1.76) and Aboriginal (aOR 1.33; 95% CI 1.08–1.64) births. When an alcohol diagnosis was recorded during pregnancy, increased odds were observed for non-Aboriginal births (aOR 2.24; 95% CI 1.09–4.60), with the highest odds of Aboriginal stillbirth occurring when an alcohol diagnosis was recorded within 1 year postpregnancy (aOR 2.88; 95% CI 1.75–4.73). The population-attributable fractions indicate that 0.8% of non-Aboriginal and 7.9% of Aboriginal stillbirths are the result of heavy alcohol consumption. Conclusions Prevention of heavy maternal alcohol use has the potential to reduce stillbirths. The lack of an association between exposure during pregnancy and Aboriginal stillbirth in this study needs further investigation.

Aim The aim of this study was to investigate the association between heavy maternal alcohol consumption and pre- peri- and postneonatally acquired cerebral palsy (CP). Method The records of all mothers with an International Classification of Diseases, revision 9 or 10 (ICD-9/-10) alcohol-related diagnostic code, indicating heavy alcohol consumption, recorded on population-based health, mental health, and drug and alcohol data sets from 1983 to 2007, and their children were identified through the Western Australian Data-linkage System. This ‘exposed’ cohort was frequency matched with mothers without an alcohol-related diagnosis and their offspring (comparison group). Cases of CP were identified through linkage with the Western Australia CP Register. Analyses were undertaken using multivariate logistic regression. Results There were 23 573 live births in the exposed group (58.6% non-Aboriginal; 41.4% Aboriginal) and 292 cases of CP. The odds of pre/perinatally acquired CP were elevated for children of non-Aboriginal mothers with an alcohol-related diagnosis recorded during pregnancy (adjusted odds ratio 3.32; 95% confidence interval [CI] 1.30–8.48) and for Aboriginal children when an alcohol-related diagnosis was recorded up to 12 months before the mother’s pregnancy (adjusted odds ratio 2.49; 95% CI 0.99–6.25). Increased odds of postneonatally acquired CP following any alcohol-related diagnosis were found for non-Aboriginal children (adjusted odds ratio 7.92; 95% CI 2.23–28.14). Interpretation These results suggest that heavy maternal alcohol consumption is a direct cause of pre/perinatally acquired CP, and an indirect cause of postneonatally acquired CP, in non-Aboriginal children. The lack of an association for Aboriginal children requires further investigation but may be due to under ascertainment of alcohol use disorders during pregnancy and other aetiological pathways.

We provided health professionals in Western Australia (WA) with educational resources about prevention of prenatal alcohol exposure and fetal alcohol spectrum disorder and assessed changes in their knowledge, attitudes and practice concerning fetal alcohol syndrome (FAS) and alcohol consumption in pregnancy. Following our 2002 survey of health professionals in WA, we developed and distributed educational resources to 3348 health professionals in WA in 2007. Six months later we surveyed 1483 of these health professionals. Prevalence rate ratios [PRR] and 95% confidence intervals [CI] were calculated to compare 2007 results with results from the 2002 survey. Of the 1001 responding health professionals, 69.8% had seen the educational resources; of these 77.1% have used them and 48.5% said the resources had assisted them to change their practice or their intention to change their practice. Compared with 2002, there was an increase in the proportion who knew all the essential features of FAS from 11.7% to 15.8% [PRR 1.35; 95% CI 1.09, 1.67] and had diagnosed FAS, from 4.8% to 7.3% [PRR 1.52; 95% CI 1.08, 2.13]. In 2007, 98.1% of health professionals stated they would advise pregnant women to consider not drinking at all or advise them that no alcohol in pregnancy is the safest choice. Health professionals surveyed in 2007 have increased their knowledge, changed their attitudes and practice about FAS, and altered the advice they give to pregnant women about alcohol consumption since our survey in 2002. It is essential that we build on this change and continue to support health professionals' knowledge, attitudes and practice about the prevention of prenatal alcohol exposure and fetal alcohol spectrum disorder. The educational resources for health professionals may be ordered as hard copies and downloaded from the internet http://www.ichr.uwa.edu.au/alcoholandpregnancy.

BACKGROUND: Use of periconceptional folic acid supplementation has been promoted in Western Australia since late 1992, and voluntary fortification of some foods with folic acid has been permitted in Australia since 1996. Reduced rates of neural tube defects (NTDs) have been observed since 1995. Aboriginal infants have a higher rate of NTDs, but no fall in rates has been documented. Encephaloceles have not been examined separately. METHODS: Data on anencephaly, spina bifida, and encephalocele were obtained from the Western Australian Birth Defects Registry. The prevalence ratio for each type of NTD was calculated, comparing 1993 to 1995 (promotion of supplements, no fortification) and 1996 to 2006 (promotion of supplements and voluntary fortification) with 1980 to 1992 (no promotion or fortification). RESULTS: From 1996 to 2006, there was a 32% reduction in anencephaly, 23% in spina bifida, and 34% in encephalocele compared with 1980 to 1992. There were no differences seen from 1993 to 1995 compared with 1980 to 1992. For Aboriginal infants, the rates were higher than for non-Aboriginal infants, for each type of NTD. The prevalence ratios, comparing 1996 to 2006 with 1980 to 1995, were 0.70 (CI, 0.61–0.79) for non-Aboriginal infants and 0.90 (CI, 0.61–1.32) for Aboriginal infants. CONCLUSIONS: Overall, the rates of encephalocele, anencephaly, and spina bifida have fallen to a similar extent in association with promotion of folic acid supplements and voluntary fortification. No such falls were seen for Aboriginal infants. These data will provide a useful baseline against which to monitor the effects of mandatory fortification on NTDs when it is introduced in Australia in September 2009. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc.

Accurate data about Indigenous child health is vital to enable us to understand its current state, to acknowledge achievements, and to determine how to reduce inequalities between Indigenous and non-Indigenous children. # We have identified a paucity of national, or nationally representative, data relating to Indigenous child health outcomes, and significant deficiencies in available data. # A coordinated national approach will help address current data limitations, including lack of identification of Indigenous status, lack of currency, and lack of information about specific health disorders affecting Indigenous children. # To ensure that health data collected are relevant and useful, Indigenous communities must have a role in data collection and management.

Neural tube defects (NTD) were 43% more common in Indigenous than in non-Indigenous infants in Western Australia in the 1980s, and there has been a fall in NTD overall in Western Australia since promotion of folate and voluntary fortification of food has occurred. In order to investigate whether the fall had occurred in both indigenous and non-Indigenous infants, data on NTD (births and terminations) were obtained from the WA Birth Defects Registry, and on all births from the Maternal and Child Health Research Data Base. Knowledge of folate was asked in a survey of indigenous women interviewed postpartum. Before the promotion of folate (1980-92), there has been a 42% increase in NTD in Indigenous compared with non-Indigenous infants (prevalence ratio (PR)=1.42 [95% confidence interval (CI) 1.04, 1.94]); while in the most recent period (1996-2000), the prevalence in Indigenous infants was almost twice that of non-Indigenous infants (PR 1.98 [CI 1.25, 3.15]). Fifty-five per cent of Indigenous women knew about folate in pregnancy. Similar to sudden infant death syndrome, this study has highlighted health promotion that has been successful in reducing the risk of a childhood condition overall, but has failed to be effective for Indigenous children.

Our Different View was stimulated by our analyses that identified very different risks of preterm birth (and most likely their outcomes) in the Aboriginal subpopulation of Western Australia. Given the increasing immigration into many wealthy countries in both North America and Europe, it is unlikely that these patterns we described are unique to Australia. Hence, our thoughts about the causes of disparities and ways to minimize them may well help others have a different view and approach to this universal paediatric issue.

Shared responsibility agreements between the Australian Government and Indigenous communities are based on a concept of mutual obligation but have overtones of paternalism and imposition. The nature and extent of choice in any such agreements need to be established.

Background Ensuring adherence to treatment and retention is important in clinical trials, particularly in remote areas and minority groups. We describe a novel approach to improve adherence, retention and clinical review rates of Indigenous children. Methods This descriptive study was nested within a placebo-controlled, randomised trial (RCT) on weekly azithromycin (or placebo) for 3-weeks. Indigenous children aged ≤24-months hospitalised with acute bronchiolitis were recruited from two tertiary hospitals in northern Australia (Darwin and Townsville). Using mobile phones embedded within a culturally-sensitive approach and framework, we report our strategies used and results obtained. Our main outcome measure was rates of adherence to medications, retention in the RCT and self-presentation (with child) to clinic for a clinical review on day-21. Results Of 301 eligible children, 76 (21%) families declined participation and 39 (13%) did not have access to a mobile phone. 186 Indigenous children were randomised and received dose one under supervision in hospital. Subsequently, 182 (99%) children received dose two (day-7), 169 (93%) dose three (day-14) and 180 (97%) attended their clinical review (day-21). A median of 2 calls (IQR 1–3) were needed to verify adherence. Importantly, over 97% of children remained in the RCT until their clinical endpoint at day-21. Conclusions In our setting, the use of mobile phones within an Indigenous-appropriate framework has been an effective strategy to support a clinical trial involving Australian Indigenous children in urban and remote Australia. Further research is required to explore other applications of this approach, including the impact on clinical outcomes. Trial registration ACTRN12608000150347 (RCT component).

Background There is little reliable information on the prevalence of fetal alcohol spectrum disorders (FASD) in Australia and no coordinated national approach to facilitate case detection. The aim of this study was to identify health professionals’ perceptions about screening for FASD in Australia. Method A modified Delphi process was used to assess perceptions of the need for, and the process of, screening for FASD in Australia. We recruited a panel of 130 Australian health professionals with experience or expertise in FASD screening or diagnosis. A systematic review of the literature was used to develop Likert statements on screening coverage, components and assessment methods which were administered using an online survey over two survey rounds. Results Of the panel members surveyed, 95 (73%) responded to the questions on screening in the first survey round and, of these, 81 (85%) responded to the second round. Following two rounds there was consensus agreement on the need for targeted screening at birth (76%) and in childhood (84%). Participants did not reach consensus agreement on the need for universal screening at birth (55%) or in childhood (40%). Support for targeted screening was linked to perceived constraints on service provision and the need to examine the performance, costs and benefits of screening. For targeted screening of high risk groups, we found highest agreement for siblings of known cases of FASD (96%) and children of mothers attending alcohol treatment services (93%). Participants agreed that screening for FASD primarily requires assessment of prenatal alcohol exposure at birth (86%) and in childhood (88%), and that a checklist is needed to identify the components of screening and criteria for referral at birth (84%) and in childhood (90%). Conclusions There is an agreed need for targeted but not universal screening for FASD in Australia, and sufficient consensus among health professionals to warrant development and evaluation of standardised methods for targeted screening and referral in the Australian context. Participants emphasised the need for locally-appropriate, evidence-based approaches to facilitate case detection, and the importance of ensuring that screening and referral programs are supported by adequate diagnostic and management capacity.

Objectives To examine alcohol-use disorders in pregnant women and the extent of under-reporting. Design Population-based cohort study. Setting Western Australia. Population Women with a birth recorded on the Western Australian Midwives Notification System (1985–2006). Methods Mothers with an International Classification of Diseases 9/10 alcohol-related diagnosis, indicating heavy alcohol consumption, recorded on population-based health datasets (non-Aboriginal n = 5839; Aboriginal n = 2583) were identified through the Western Australian data-linkage system. This ‘exposed’ cohort was frequency matched (on maternal age, year of birth of offspring, Aboriginal status) with comparison mothers without an alcohol-related diagnosis (non-Aboriginal n = 33 979; Aboriginal n = 8005). Main outcome measures Trends in maternal alcohol diagnoses in relation to pregnancy for non-Aboriginal and Aboriginal women. The proportion of children diagnosed with fetal alcohol syndrome (FAS) who had a mother with an alcohol diagnosis recorded during pregnancy. Results The proportion of Aboriginal mothers in Western Australia with an alcohol diagnosis (23.1%) is ten times greater than for non-Aboriginal mothers (2.3%). There has been a six-fold increase in the percentage of non-Aboriginal births with a maternal alcohol diagnosis recorded during pregnancy and a 100-fold increase for Aboriginal births. Around 70% of the mothers of children diagnosed with FAS did not have an alcohol diagnosis recorded during pregnancy and 18% of the mothers had no record of an alcohol diagnosis. Conclusions Maternal alcohol exposure during pregnancy is significantly under-ascertained. Given the severe risks to the fetus from heavy prenatal alcohol exposure, assessment and recording of alcohol use should be routinely undertaken in maternity and other health settings.

The aim of this study was to examine the association between maternal alcohol use disorder and intellectual disability in children.All mothers with an International Classification of Diseases (ICD) 9 and/or 10 alcohol-related diagnosis, a proxy for alcohol use disorder, recorded on the Western Australian health, mental health, and drug and alcohol data sets were identified through the Western Australian Data Linkage Unit (n=5614 non-Aboriginal; n=2912 Aboriginal). A comparison cohort of mothers without an alcohol-related diagnosis was frequency matched on maternal age within maternal Aboriginal status and year of birth of their children. Linkage with the Western Australian Midwives Notification System (1983-2001) identified all births to these mothers (n=10 664 and 7907 respectively). Linkage to the Western Australian Intellectual Disability Database and Register of Developmental Anomalies identified cases of intellectual disability with no identified genetic origin (intellectual disability) (n=1487) and fetal alcohol syndrome (n=66). Odds ratios (ORs) and 95% confidence intervals (CIs) for intellectual disability were calculated using logistic regression incorporating generalized estimating equations and used to estimate population-attributable fractions.At least 3.8% (95% CI 2.84-4.89%) of cases of intellectual disability could be avoided by preventing maternal alcohol use disorder: 1.3% (95% CI 0.81-1.86%) in non-Aboriginal and 15.6% (95% CI 10.85-20.94%) in Aboriginal children. We observed a three-fold increase in the adjusted odds of intellectual disability in children of mothers with an alcohol-related diagnosis recorded during pregnancy (non-Aboriginal OR 2.89, 95% CI 1.62-5.18; Aboriginal OR 3.12, 95% CI 2.13-4.56), with a net excess proportion of 3.7% and 5.5% respectively. One-third (32%) of children diagnosed with fetal alcohol syndrome had intellectual disability.Maternal alcohol use disorder is the leading known risk factor for intellectual disability with no identified genetic origin.

Objective In September 2009, Australia implemented mandatory folic acid fortification of wheat flour for bread-making to reduce the incidence of neural tube defects. Our study aimed to establish baseline folate status data in Aboriginal and non-Aboriginal Western Australians. Methods Patients who presented at a health service or collection centre for blood tests were invited to participate. One hundred and ninety-one Aboriginals and 159 non-Aboriginals were recruited between April 2008 and September 2009. Participants completed a five-minute questionnaire and had blood taken for red blood cell (RBC) folate and serum vitamin B12. Data were analysed using SPSS (version 17.0.2, SPSS Inc., Chicago, IL, USA). Results Ten per cent (95% confidence intervals (CI): 5, 19) of the Aboriginal women participants and 26% (95% CI: 16, 40) of men had RBC folate concentrations below 250 ng/mL, the cut-off associated with folate deficiency. None of the non-Aboriginal women (95% CI: 0, 4) and 4% of the non-Aboriginal men (95% CI: 2, 12) had RBC folate concentrations below 250 ng/mL. All participants were vitamin B12 replete. None of the 96 Aboriginal and 8% of non-Aboriginal women aged 16–44 reported consumption of supplements with a daily intake of >400 μg folic acid during the previous week. Conclusions and implications This study established a baseline of RBC folate, folate consumption and supplement use in Aboriginal and non-Aboriginal groups. We identified 10% of Aboriginal women and none of non-Aboriginal women participants with low folate concentrations. The higher prevalence of folate deficiency in Aboriginal participants suggests they are more likely to benefit from a universal program of folate fortification.

The aim of this study was to investigate the association between heavy maternal alcohol consumption and pre- peri- and postneonatally acquired cerebral palsy (CP).The records of all mothers with an International Classification of Diseases, revision 9 or 10 (ICD-9/-10) alcohol-related diagnostic code, indicating heavy alcohol consumption, recorded on population-based health, mental health, and drug and alcohol data sets from 1983 to 2007, and their children were identified through the Western Australian Data-linkage System. This 'exposed' cohort was frequency matched with mothers without an alcohol-related diagnosis and their offspring (comparison group). Cases of CP were identified through linkage with the Western Australia CP Register. Analyses were undertaken using multivariate logistic regression.There were 23 573 live births in the exposed group (58.6% non-Aboriginal; 41.4% Aboriginal) and 292 cases of CP. The odds of pre/perinatally acquired CP were elevated for children of non-Aboriginal mothers with an alcohol-related diagnosis recorded during pregnancy (adjusted odds ratio 3.32; 95% confidence interval [CI] 1.30-8.48) and for Aboriginal children when an alcohol-related diagnosis was recorded up to 12 months before the mother's pregnancy (adjusted odds ratio 2.49; 95% CI 0.99-6.25). Increased odds of postneonatally acquired CP following any alcohol-related diagnosis were found for non-Aboriginal children (adjusted odds ratio 7.92; 95% CI 2.23-28.14).These results suggest that heavy maternal alcohol consumption is a direct cause of pre/perinatally acquired CP, and an indirect cause of postneonatally acquired CP, in non-Aboriginal children. The lack of an association for Aboriginal children requires further investigation but may be due to under ascertainment of alcohol use disorders during pregnancy and other aetiological pathways.

The authors review results from a study in Western Australia of stress exposure and resilience among Aboriginal children and young people who come from families where there is violence. The findings are provocative given the social and economic marginalization the youth face. Results show that the youth who are the most resilient are those who report less adherence to their culture and come from lower rather than higher socioeconomic households.

Background To explore women's alcohol consumption in pregnancy, and potential predictors of alcohol consumption in pregnancy including: demographic characteristics; and women's knowledge and attitudes regarding alcohol consumption in pregnancy and its effects on the fetus. Methods We conducted a national cross-sectional survey via computer assisted telephone interview of 1103 Australian women aged 18 to 45 years. Participants were randomly selected from the Electronic White Pages. Pregnant women were not eligible to participate. Quotas were set for age groups and a minimum of 100 participants per state to ensure a national sample reflecting the population. The questionnaire was based on a Health Canada survey with additional questions constructed by the investigators. Descriptive statistics were calculated and logistic regression analyses were used to assess associations of alcohol consumption in pregnancy with participants' characteristics, knowledge and attitudes. Results The majority of women (89.4%) had consumed alcohol in the last 12 months. During their last pregnancy (n = 700), 34.1% drank alcohol. When asked what they would do if planning a pregnancy (n = 1103), 31.6% said they would consume alcohol and 4.8% would smoke. Intention to consume alcohol in a future pregnancy was associated with: alcohol use in the last pregnancy (adjusted OR (aOR) 43.9; 95% Confidence Interval (CI) 27.0 to 71.4); neutral or positive attitudes towards alcohol use in pregnancy (aOR 5.1; 95% CI 3.6 to 7.1); intention to smoke in a future pregnancy (aOR 4.7; 95% CI 2.5 to 9.0); and more frequent and higher current alcohol consumption. Conclusions Women's past pregnancy and current drinking behaviour, and attitudes to alcohol use in pregnancy were the strongest predictors of alcohol consumption in pregnancy. Targeted interventions for women at higher risk of alcohol consumption in pregnancy are needed to change women's risk perception and behaviour.

Background Alcohol exposure in pregnancy is a common and modifiable risk factor for poor pregnancy and child outcomes. Alcohol exposure in pregnancy can cause a range of physical and neurodevelopmental problems in the child including the Fetal Alcohol Spectrum Disorders (FASD). In order to improve prevention strategies, we sought to describe the knowledge and attitudes of women of childbearing age regarding alcohol consumption during pregnancy and its effects on the fetus. Methods We conducted a national cross-sectional survey via computer assisted telephone interview of 1103 Australian women aged 18 to 45 years. Participants were randomly selected from the Electronic White Pages. Pregnant women were not eligible to participate. Quotas were set for age groups and a minimum of 100 participants per state to ensure a national sample reflecting the population. The questionnaire was based on a Health Canada survey with additional questions constructed by the investigators. Descriptive statistics were calculated and logistic regression analyses were used to assess associations with participants' knowledge and attitudes. Results Of women surveyed, 61.5% had heard about effects of alcohol on the fetus and 55.3% had heard of Fetal Alcohol Syndrome. Although 92.7% agreed alcohol can affect the unborn child, 16.2% did not agree that the disabilities could be lifelong. Most women agreed that pregnant women should not drink alcohol (80.2%) and 79.2% reported having negative feelings towards pregnant women drinking alcohol. Women with higher education levels were more likely to know the effects of alcohol consumption in pregnancy (adjusted OR 5.62; 95% CI 3.20 to 9.87) but education level and knowledge were not associated with attitude. Conclusions There was a disjunction between knowledge and attitudes towards alcohol consumption in pregnancy. These findings will assist in developing effective health promotion campaigns to reduce fetal alcohol exposure and subsequent fetal damage.

Health professionals have an important role to play in preventing prenatal alcohol exposure. In 2006 qualitative data were collected from 53 health professionals working in primary care in metropolitan and regional Western Australia. Thematic analysis was used to elucidate barriers in addressing prenatal alcohol use and the strategies used to overcome them. Health professionals identified strategies for obtaining alcohol use information from pregnant women but they are not recognizing moderate alcohol intake in pregnant women. Study limitations are noted and the implications of the results are discussed. This research was funded by the Health Promotion Foundation of Western Australia.

Objective To describe the role that alcohol plays in the lives of Aboriginal people living with HIV in Western Australia. Methods Semi-structured interviews were conducted between February and September 2003 with 20 Aboriginal people who were HIV-positive; almost half the total number of Aboriginal people known to be living with HIV in Western Australia at that time. The main purpose of the study was to document their experiences of living with HIV and aspects of health service delivery. Results Drinking emerged as a key theme in the majority of interviews. Alcohol had a major role in disinhibition and risk-taking behaviour of both the participants and those they socialised with. It was perceived as a commodity, a way of altering reality, and a pathway through which social connection was maintained and was central to the common narratives of loss, chaos and transformation. Post-diagnosis, alcohol helped with disclosure and temporary blunting of distress as a result of the HIV diagnosis. It also contributed to a lack of capacity to comply with anti-retroviral therapy although narratives also included personal growth and restoration of physical health. Conclusions Effective strategies to reduce risk of STIs and HIV and prevent other health problems need to address substance use issues but this also requires amelioration of the structural inequalities that make minority groups vulnerable.