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Background: The teratogenic effects of maternal alcohol consumption during pregnancy include anomalies of craniofacial structures derived from the cranial neural crest cells. The presence of specific craniofacial anomalies contributes to the diagnosis of fetal alcohol spectrum disorders. Cleft lip and palate [orofacial clefts (OFCs)], also derived from the cranial neural crest cells, are common congenital anomalies, but their relationship with prenatal alcohol consumption is unknown., Methods: To evaluate the association between maternal consumption of alcohol during pregnancy and the occurrence of OFCs in infants, we conducted a systematic review and meta-analyses of published studies. We examined the associations between any alcohol consumption, binge level drinking, and heavy and moderate levels of consumption vs. no or low levels of consumption., Results: After screening 737 publications, we identified 33 studies (23 case-control and 10 cohort studies). There was considerable heterogeneity in individual study design, quality measures and study results. Findings from random effects meta-analyses suggest no relationship between prenatal alcohol consumption and the occurrence of OFCs {pooled odds ratios for any alcohol intake and binge level drinking respectively: cleft lip with or without cleft palate 1.00 [95% confidence interval (CI) 0.86, 1.16] from 18,349 participants in 13 studies, 1.04 [95% CI 0.87, 1.24] [8763 individuals, 4 studies]; cleft palate only 1.05 [95% CI 0.92, 1.21] [21,459 individuals, 17 studies], 0.94 [95% CI 0.74, 1.21] [7730 participants, 4 studies]}., Conclusions: While we found no association between alcohol consumption during pregnancy and OFCs in infants, the influence of study design, particularly in relation to alcohol exposure measurement and OFC ascertainment cannot be ignored., (© 2014 John Wiley & Sons Ltd.)

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 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., (© The Authors. Developmental Medicine & Child Neurology © 2012 Mac Keith Press.)

The objective was to evaluate the Alcohol and Pregnancy Project that provided health professionals in Western Australia (WA) with educational resources to inform them about prevention of prenatal alcohol exposure and fetal alcohol spectrum disorder (FASD). The authors developed, produced, and distributed educational resources to 3,348 health professionals in WA. Six months later, they surveyed 1,483 of these health professionals. The authors used the RE-AIM framework (reach, effectiveness, adoption, implementation, and maintenance) to evaluate the project. The educational resources were effective in producing a 31% increase in the proportion of health professionals who routinely provided pregnant women with information about the consequences of drinking alcohol during pregnancy. One hundred percent of the settings adopted the project, it reached 96.3% of the target population, it was implemented as intended, and the resources were maintained (http://www.ichr.uwa.edu.au/alcoholandpregnancy). The educational resources for health professionals have potential to contribute to reducing prenatal alcohol exposure and FASD.

Background: When examining the association between prenatal alcohol exposure and fetal effects, the timing and intensity of exposure have been ignored in epidemiological studies. The effect of using dose, pattern and timing of consumption ("composite" method) was investigated in this study, to examine the association between prenatal alcohol exposure and fetal effects., Methods: The composite method resulted in six categories of exposure (abstinent, low, moderate, binge

Objective: The goal was to examine the associations between dose, pattern, and timing of prenatal alcohol exposure (PAE) and birth defects., Methods: Data from a randomly selected, population-based cohort of nonindigenous women who gave birth to a live infant in Western Australia (WA) between 1995 and 1997 (N=4714) were linked to WA Midwives Notification System and WA Birth Defects Registry data. We assessed the associations of PAE before pregnancy, in the first trimester, and in late pregnancy with any birth defect and with birth defects classified as alcohol-related birth defects (ARBDs) by the Institute of Medicine (IOM), by using logistic regression., Results: The prevalence of birth defects classified as ARBDs by the IOM was low. Compared with abstinence, heavy PAE in the first trimester was associated with increased odds of birth defects classified as ARBDs (adjusted odds ratio: 4.6 [95% confidence interval: 1.5-14.3]), with similar findings after validation through bootstrap analysis. There was no association between low or moderate PAE and birth defects., Conclusions: A fourfold increased risk of birth defects classified as ARBDs was observed after heavy PAE in the first trimester. Many individual birth defects included in the IOM classification for ARBDs either were not present in this cohort or were not associated with PAE. Large, population-based studies are needed to strengthen the evidence base for ARBDs.

Background: There is a lack of evidence regarding the effect of dose, pattern and timing of prenatal alcohol exposure and behaviour problems in children aged 2 years and older., Methods: A 10% random sample of women delivering a live infant in Western Australia (1995-96) were invited to participate in an 8-year longitudinal survey (78% response rate n = 2224); 85% were followed-up at 2 years, 73% at 5 years and 61% at 8 years. Alcohol consumption was classified by combining the overall dose, dose per occasion and frequency to reflect realistic drinking patterns. Longitudinal analysis was conducted using generalized estimating equations (GEE) to investigate the association between child behaviour as measured by the Child Behaviour Checklist at 2, 5 and 8 years of age and prenatal alcohol exposure collected 3 months postpartum for each trimester separately, adjusting for a wide range of confounding factors., Results: Low levels of prenatal alcohol were not associated with child behaviour problems. There were increased odds of internalizing behaviour problems following heavy alcohol exposure in the first trimester; anxiety/depression [adjusted odds ratio (aOR) 2.82; 95% confidence interval (CI) 1.07-7.43] and somatic complaints (aOR 2.74; 95% CI 1.47-5.12) and moderate levels of alcohol exposure increased the odds of anxiety/depression (aOR 2.24; 95% CI 1.16-4.34)., Conclusions: Prenatal alcohol exposure at moderate and higher levels increased the odds of child behaviour problems with the dose, pattern and timing of exposure affecting the type of behaviour problems expressed. Larger studies with more power are needed to confirm these findings.