Foetal alcohol spectrum disorder (FASD) is a set of symptoms and signs that may follow from exposure of the unborn child to alcohol during pregnancy. Characterised by cognitive and behavioural impairments, one secondary outcome from FASD, is encounters with the criminal justice system (CJS). In some countries, for example, England and Wales, it seems likely that many cases are missed at this point and, thus, courts are at risk of making unsafe judgements. We could learn a lot from countries where services are generally more used to dealing with FASD. Australia is one such country.

Prenatal alcohol exposure causes disruptions in brain development. The resulting disorder, fetal alcohol spectrum disorder (FASD), cannot be cured, but interventions can help improve the daily functioning of affected children and adolescents and the quality of life for the entire family.The aim of the German guideline version 2024 is to provide validated and evidence-based recommendations on interventions for children and adolescents with FASD.We searched for international guidelines and performed a systematic literature review and a hand search to identify literature (published 2012-2022) on interventions for children (0-18 years) with FASD. The quality of the literature was assessed for predefined outcomes using the GRADE method (grading of recommendations, assessment, development, and evaluation). We established a multidisciplinary guideline group, consisting of 15 professional societies, a patient support group, and 10 additional experts in the field. The group agreed on recommendations for interventions based on the systematic review of the literature and formulated additional recommendations, based on clinical experience/expert evidence in a formal consensus process.No international guideline focusing on interventions for patients with FASD was found. Thirty-two publications (4 systematic reviews and 28 original articles) were evaluated. The analysis resulted in 21 evidence-based recommendations and 26 expert consensus, covering the following topics: neuropsychological functioning, adverse effects of therapy, complications/secondary conditions, quality of life, caregiver burden, knowledge of FASD, and coping and self-efficacy.The German guideline is the first internationally to provide evidence-based recommendations for interventions in children and adolescents with FASD.

Fetal Alcohol Spectrum Disorder (FASD) is a lifelong neurodisability caused by exposure to alcohol in utero. It can have a severe impact on the affected child as well as their families, yet the costs associated are unclear. This scoping review sought to identify the costs associated with raising a child with FASD.

A database search was conducted in July 2024 on PubMed, Scopus, Ovid Medline and Web of Science, searching for all empirical research on the "cost" to "caregivers" of raising a child with "FASD". Articles were excluded if they did not outline the costs of FASD, or the effects of prenatal alcohol exposure, or if they did not contain parent/caregiver response. After the removal of duplicates, 421 unique articles were found based on the search criteria. Just three articles met the inclusion/exclusion criteria. Two additional publications were identified through citation checking. Thus, five articles were included in this review. Thematic analysis was used to interpret the findings and synthesise the results.

Personal costs ranged between USD$198.13-CAD$6215,27 per person per year. These articles identified that parents incurred costs related to medical care, education, social services, productivity losses, externalising behaviours, other direct costs to the family, and psychosocial impacts on families. Differences were considered in relation to the child's age, age at the time of diagnosis, severity of disability, relationship to caregiver, location, and other demographic factors.

More research is needed to provide a more accurate estimate of the cost of raising a child with FASD.

People with fetal alcohol spectrum disorder (FASD) can experience a range of individual, social, and systemic challenges that may increase the likelihood of life adversity, including contact with the criminal legal system (CLS). The purpose of this article was to update a 2018 systematic review of literature on this intersection of FASD and the CLS. We searched ten academic databases for studies with people with FASD involved in the CLS, as well as caregivers and service providers who support them. A total of 54 studies were identified, published between April 2017 and March 2024, which is more than double what was present in 2018. Most of this research was conducted in Canada and Australia with individuals with FASD across the lifespan. These studies indicate growth in the literature on FASD prevalence in CLS settings (n = 3), CLS-related trajectories for people with FASD (n = 15), the needs and strengths of people with FASD involved in the CLS (n = 9), FASD-informed CLS responses (n = 17), and CLS professional knowledge, attitudes, and practices related to FASD (n = 10). Despite these advancements, there remain limitations in the evidence base such as a lack of specific and rigorous intervention studies; longitudinal research on outcomes and trajectories; generalizable prevalence estimates; the unique ways in which needs, risk, and protective factors may be experienced by people with FASD; how socio-cultural factors impact people with FASD and the research conducted in this area; as well as training opportunities for professionals supporting those with FASD in the CLS. These findings are integrated with results reported in the 2018 review to identify priority areas for future research.

Fetal alcohol spectrum disorder (FASD) is a neurodevelopmental disorder associated with prenatal alcohol exposure (PAE). In Australia, there are several barriers to assessment, including a limited number of FASD-informed clinicians. This study aimed to understand the perspectives of psychologists, parents, caregivers, and adults with FASD on the current assessment process, as well as methods to improve FASD training and universal screening of PAE.

Two groups of (1) psychologists and (2) parents, caregivers, and adults with FASD were interviewed about their experiences of FASD assessment and their recommendations for training and universal screening of PAE. Thematic analysis was employed to code data.

Five key themes were identified: (1) stigma and stereotypes of PAE, (2) support for universal screening of PAE, (3) differential, co-occurring, and missed diagnoses, (4) lack of support following diagnosis, and (5) need for improved training for psychologists. Stereotypes of women who drink were present across themes, with both groups discussing the importance of PAE assessment for all women during antenatal care and when presenting for assessment of neurodevelopmental disorders. The importance of training more FASD-informed clinicians who can understand the uniqueness of each individual with FASD was highlighted, with hopes of improving diagnostic capacity as well as support offered by psychologists.

Recognition of the impact of PAE is growing in Australia; however, there is a need to embed this topic within university training for psychologists.

This systematic review aims to investigate craniofacial symptoms, oral healthcare requirements, and management approaches for children diagnosed with Fetal Alcohol Spectrum Disorder (FASD).

Electronic searches were conducted across five databases (PubMed, Embase, Cochrane Library, Scopus, Web of Science, and LILACS). The inclusion criteria focused on original research for children with FASD, up to 18 years, emphasizing craniofacial symptoms, oral health, and management protocols. Data extraction was performed independently by two researchers using predetermined criteria. The JBI Critical Appraisal Tool was used to assess the risk of bias in the selected studies. PICO criteria guided study selection, with a focus on low risk of bias. Data analysis was carried out independently by two researchers.

Among 361 identified papers, 215 were screened, and 16 studies meeting research criteria were included. The findings established a body of evidence linking characteristic craniofacial symptoms to FASD. They highlighted heightened oral health needs for children with FASD, emphasizing the significance of frequent recall and preventive measures.

This review solidifies the connection between maternal alcohol consumption during pregnancy and dentofacial complications in children with FASD, including cleft lip/palate, malocclusion, increased DMFT, and craniofacial dysmorphia. It underscores the pivotal role of pediatric dentists in early identification and intervention.

Prenatal ethanol exposure (PE) causes Fetal Alcohol Spectrum Disorders (FASD), characterized by cognitive, behavioral, and emotional deficits, including anxiety and depression. PE-induced alteration in the function of dorsal raphe nucleus (DRN) serotonin (5-HT) neurons is thought to be major contributing factor for increased anxiety. However, the precise neuronal circuits involved are unknown. Using electrophysiology, optogenetics, chemogenetics, and behavioral approaches, we find that PE preferentially potentiates medial prefrontal cortex (mPFC) glutamatergic inputs, but not lateral habenula (LHb), to DRN 5-HT neurons projecting to mPFC. Additionally, PE also increases the strength of LHb but not mPFC excitatory inputs to DRN 5-HT neurons projecting to central amygdala (Ce). This input and target selective effect of PE was mediated by a circuit-specific increase in nitric oxide (NO) signaling. Importantly, chemogenetic inhibition of mPFC-DRN neuronal circuit blunted anxiety-like behaviors in PE rats. As such, our results unraveled the DRN neuronal circuitries affected by PE, which gate FASD-induced anxiety-like behaviors.

Fetal alcohol spectrum disorders (FASDs) are associated with neurocognitive deficits for which there are no biological treatments. Choline supplementation may attenuate these deficits.

This study was aimed to evaluate choline as a neurodevelopmental intervention for preschool-aged children with FASD.

We present combined data from 104 participants with FASD (aged 2.5-5.9 y) from 3 placebo randomized controlled trials (RCTs). Participants in RCT1 and RCT2 were randomly assigned to 9 mo choline (500 mg daily) or placebo. Participants in RCT3 were randomly assigned to 9 mo choline (19 mg/kg daily) or placebo. The primary outcome measure was an elicited imitation (EI) memory task.

Adherence was high (78% doses received). Adverse effects were similar across groups except fishy body odor: choline group, 36%; placebo group, 8%. We observed a trend-level choline advantage; participants receiving choline performed 25% better on EI short-delay adjacent pairs (sequential memory) than those on placebo, with a steeper increase in scores between 6 and 9 mo (ŷ = -10.06; P = 0.03; 95% CI: -19.13, -0.99). No sex difference in response was seen, nor did we observe a dose-response relationship. Age-moderated response to choline between baseline and 9 mo (ŷ = 10.02; P = 0.01; 95% CI: 2.47, 17.57), with greater response in younger (≤4.2 y) than that in older (>4.2 y) participants. Overall, choline showed a beneficial effect on memory but no impact on executive functioning or intelligent quotient.

The results support choline as a neurodevelopmental intervention for improvement of memory in young children exposed to alcohol prenatally. Specifically, the use of choline bitartrate as a supplement in the range of 260-500 mg/d in children between 2.5 and 5.9 y of age is supported. Future studies are needed to further define appropriate dosage as well as optimal lengths and developmental windows for supplementation. This trial was registered at clinicaltrials.gov as NCT01149538 and NCT02735473.

IntroductionPediatric neurology provides care for children with complex developmental disorders with environmental, genetic, metabolic, and teratogenic etiologies. Common neurodevelopmental conditions include attention-deficit hyperactivity disorder (ADHD), and autism spectrum disorder. However, only minimal attention from pediatric neurology journals has been devoted to fetal alcohol spectrum disorder. This is surprising because fetal alcohol spectrum disorder is a common neurodevelopmental disorder with a prevalence of between 1% and 5% of school-age children.MethodsThis scoping review had 2 objectives. Objective 1 was to estimate the number of articles reporting on fetal alcohol spectrum disorder in 8 well-respected pediatric neurology journals. Objective 2 was to determine how many patients from a single pediatric neurology practice referred to a clinic for diagnosis and management of neurobehavioral disorders received a diagnosis of ADHD, autism spectrum disorder, and fetal alcohol spectrum disorder.ResultsObjective 1, a survey of 8 prominent pediatric neurology journals until January 2024, found that a title and abstract search identified 1786 articles on the three topics. Papers on autism spectrum disorder (n =1043) accounted for 58.4% of the total. Papers on ADHD (n = 685) comprised 38.4% and articles on fetal alcohol spectrum disorder (n = 58) contributed just 3.3% of the total.Objective 2, a chart review of 40 patients from a single pediatric neurology clinic who were referred for developmental assessment and management, found that 40% had prenatal alcohol exposure and 20% received a diagnosis of fetal alcohol spectrum disorder. High rates of comorbidity between fetal alcohol spectrum disorder and ADHD of 21% and of fetal alcohol spectrum disorder and autism spectrum disorder of 2.5% were found.ConclusionsBecause fetal alcohol spectrum disorder is one of the most common causes of neurodevelopmental disorders, the limited attention to fetal alcohol spectrum disorder in pediatric neurology journals is concerning. This study suggests that in addition to ADHD and autism spectrum disorder, fetal alcohol spectrum disorder may also be a common diagnosis in pediatric neurology practice. Pediatric neurology journals may need to take active steps to increase content on fetal alcohol spectrum disorder. This could include editorials, invited commentaries, or topical reviews. Early recognition and diagnosis of fetal alcohol spectrum disorder allows for the implementation of specific interventions, which can improve the quality of life for patients and families.

We investigated the molecular and clinical profile of five boys carrying the fragile X messenger ribonucleoprotein 1 (FMR1) mutation and who suffered from the effects of prenatal alcohol exposure. Fragile X syndrome (FXS) testing was performed using PCR and Southern Blot analysis, and fragile X messenger ribonucleoprotein protein (FMRP) expression levels were measured by Western blot analysis. Clinical evaluation included cognitive functions, adaptive skills, autism phenotype, and severity of behavior measures. Fetal Alcohol Spectrum Disorder (FASD) was also assessed. Five adopted male siblings were investigated, four of which (cases 1, 2, 3, and 4) were diagnosed with FXS, FASD, and ASD, and one, the fraternal triplet (case 5), was diagnosed with FASD and ASD and no FXS. The molecular profile of case 1 and 2 showed the presence of a hypermethylated full mutation (FM) and the resulting absence of FMRP. Cases 3 and 4 (identical twins) were FM-size mosaics (for the presence of an FM and a deleted allele), resulting in 16% and 50% FMRP expression levels, respectively. FMRP expression level was normal in case 5 (fraternal twin). Severe behavioral problems were observed in all cases, including aggression, tantrum, self-harming, anxiety, and defiant behavior, due to different mutations of the FMR1 gene, in addition to biological exposure, home environmental factors, and potentially to additional background gene effects.

Delayed motor development is an early clinical sign of Fetal Alcohol Spectrum Disorders (FASD). However, changes at the neural circuit level that underlie early motor differences are underexplored. The striatum, the principal input nucleus of the basal ganglia, plays an important role in motor learning in adult animals, and the maturation of the striatal circuit has been associated with the development of early motor behaviors. Here, we briefly exposed pregnant C57BL/6 dams to ethanol (5% w/w) in a liquid diet on embryonic days (E)13.5-16.5, and assessed the mouse progeny using a series of 9 brief motor behavior tasks on postnatal days (P)2-14. Live brain slices were then obtained from behaviorally-tested mice for whole cell-voltage and current clamp electrophysiology to assess GABAergic/glutamatergic synaptic activity, and passive/active properties in two populations of striatal neurons: GABAergic interneurons and spiny striatal projection neurons. Electrophysiologically-recorded spiny striatal projection neurons were also filled intracellularly with biocytin for post-hoc analysis of dendritic morphology. We found that prenatal ethanol exposure resulted in developmental motor delays that were more severe in male mice and coincided with sex-dependent differences in the maturation of striatal neurons. Our findings indicate that prenatal ethanol exposure results in dynamic morphological and functional changes to the developmental trajectories of striatal neurons commensurate with the development of motor behaviors that differ between male and female mice.Significance Statement Developmental differences in motor behaviors are an early clinical sign of Fetal Alcohol Spectrum Disorders (FASD) but the neural circuit level changes that contribute to these differences have not yet been determined. Here we demonstrate that a brief binge exposure to ethanol alters the motor development of neonatal mice in a sex-dependent manner, and identify concurrent differences in the functional, synaptic and morphological development of striatal GABAergic interneurons and medium spiny striatal projection neurons. These data suggest that altered development of striatal neurons may contribute to differences in early motor development observed in individuals with FASD.

Fetal alcohol spectrum disorder (FASD) is a developmental disability. A diagnosis of FASD is vital for support and wellbeing. However, receiving a diagnosis can be challenging. The aim of this research was to understand the experiences and impact of diagnosis for caregivers of those with FASD in New Zealand.

We conducted focus groups with caregivers and whānau (family) to explore their experiences with FASD. The transcripts were analysed using reflexive thematic analysis.

We identified three themes across the life course of diagnosis, barriers to diagnosis, meaning of diagnosis and life with diagnosis.

A diagnosis is vital for caregivers of those with FASD. However, it is difficult to access a diagnosis in New Zealand due to professionals' lack of training, knowledge, and inadequate professional support. It is essential to build our professionals workforce competence and skills of FASD.

Alcohol consumption during pregnancy poses serious risks to maternal and fetal health, making it a public health concern. This study sheds light on the sociodemographic disparities linked to alcohol use among pregnant women in Brazilian capital cities, highlighting vulnerable groups and regional variations. These findings underscore the urgent need to develop tailored preventive strategies to protect maternal and child health. ■ Any alcohol consumption during pregnancy: prevalence of 11.5%. ■ Excessive alcohol consumption during pregnancy: prevalence of 3.0%. ■ Risk factors: older age, low education, and Indigenous ethnicity. ■ Protective factors: being married and living in Northern Brazil.

To analyze the prevalence and factors associated with alcohol consumption among pregnant women.

This cross-sectional study examined pregnant women living in Brazilian capitals using information collected by the Noncommunicable Chronic Disease Risk Factor Surveillance System (Vigitel) between 2006 and 2021. This study calculated the prevalence of both excessive and any amount of alcohol consumption by pregnant women and their associations with sociodemographic variables. Multivariate analysis was performed with prevalence ratios based on Poisson crude and adjusted regressions; the threshold for statistical significance was set at p<0.05.

The sample comprised 4,734 pregnant women. The prevalence of any amount of alcohol consumption was 11.5% (95%CI = 9.8-13.6), and that of excessive consumption was 3.0% (95%CI = 2.1-4.2); both remained stable throughout the analyzed period. Being 35-54 years old and having low educational attainment were the main factors associated with both consumption patterns. Being Indigenous was highly associated only with excessive alcohol consumption, whereas being legally married and living in Northern Brazil were protective factors.

These findings emphasize the need for focused preventive strategies targeting the most vulnerable groups to mitigate alcohol consumption and its associated risks during pregnancy.

Fetal alcohol spectrum disorder (FASD) is a highly prevalent neurodevelopmental disability caused by prenatal alcohol exposure (PAE). Healthcare professionals (HCP) are key in prevention, diagnosis, and supporting individuals with FASD. This study explored the FASD knowledge, attitudes, and practices among HCP in Aotearoa, New Zealand (NZ).

We conducted an online survey of HCP working in NZ. The survey measured knowledge of FASD, beliefs and attitudes about FASD, experiences and practices with FASD and future training.

Of the 96 participants, more than 90% self-reported a good or very good understanding of FASD, and around half had a patient with FASD. However, less than half felt prepared to support someone with FASD. Participants identified lack of professional training, services, and funding as barriers to support individuals with FASD.

We identified a need to provide training and promote awareness and recognition for HCP to support individuals with FASD.

Prenatal alcohol exposure increases the risk of congenital heart diseases (CHDs) by disrupting fetal development, yet the mechanisms underlying alcohol-induced cellular and molecular changes in human cardiogenesis remain unclear. This study investigates the effects of ethanol exposure on cardiomyocyte differentiation using human induced pluripotent stem cells (hiPSCs) as a model. Cardiomyocyte differentiation was induced using Wnt signaling molecules, and hiPSCs were treated with ethanol at concentrations of 17, 50, and 100 mM from day 0 to day 12. Ethanol treatment impaired cardiac differentiation efficiency in the early stage (days 5-7) and reduced cell proliferation in the late stage (days 12-13) in a dose-dependent manner, resulting in fewer cardiac progenitors and cardiomyocytes. Additionally, ethanol exposure caused mitochondrial defects, characterized by redox imbalance, reduced membrane potential, and decreased mitochondrial content and cellular respiration. Proteomic analysis revealed downregulation of proteins involved in calcium binding and fatty acid oxidation, a key metabolic pathway for cardiac development. These findings shed light on the mechanisms by which alcohol disrupts cardiomyocyte differentiation and may inform strategies to mitigate alcohol-induced CHD risk.

Background: Prenatal alcohol exposure (PAE) models can cause neurodevelopmental abnormalities like those observed in fetal alcohol spectrum disorder (FASD). Previous studies link experimental PAE effects in the brain to impaired signaling through insulin/IGF and Notch pathways that mediate neuronal survival, growth, migration, energy metabolism, and plasticity. Importantly, concurrent administration of peroxisome proliferator-activated receptor agonists or dietary soy prevented many aspects of FASD due to their insulin-sensitizing, anti-inflammatory, and antioxidant properties. Objective: To determine if dietary soy interventions during pregnancy would be sufficient to normalize central nervous system structure and function, we examined the effects of maternal gestation-limited dietary soy on cerebellar postnatal development, motor function, and critical signaling pathways. Methods: Pregnant Long Evans rats were fed isocaloric liquid diets containing 0% or 26% caloric ethanol with casein or soy isolate as the protein source. The ethanol and soy feedings were discontinued upon delivery. The offspring were subjected to rotarod motor function tests, and on postnatal day 35, they were sacrificed to harvest cerebella for histological and molecular studies. Results: Despite the postnatal cessation of alcohol exposure, chronic gestational exposure reduced brain weight, caused cerebellar hypoplasia, and impaired motor performance. Gestational dietary soy prevented the ethanol-associated reduction in brain weight and largely restored the histological integrity of the cerebellum but failed to normalize motor performance. Ethanol withdrawal abolished the impairments in insulin/IGF signaling that were previously associated with ongoing ethanol exposures, but ethanol's inhibitory effects on Notch and Wnt signaling persisted. Soy significantly increased cerebellar expression of the insulin and IGF-1 receptors and abrogated several ethanol-associated impairments in Notch and Wnt signaling. Conclusions: Although gestation-restricted dietary soy has significant positive effects on neurodevelopment, optimum prevention of FASD's long-term effects will likely require dietary soy intervention during the critical periods of postnatal development, even after alcohol exposures have ceased.

Many women consume alcohol while pregnant before they are aware of the pregnancy, raising concerns about potential harms to the developing fetus. Official guidelines in the United Kingdom recommend abstinence throughout pregnancy, and many women turn to online forums for reassurance and information. However, online forums can also become a source of misinformation, potentially increasing confusion and anxiety among women who have consumed alcohol before pregnancy awareness. This study explored discussions about alcohol consumption before pregnancy awareness on Mumsnet to understand the nature of peer response and assess the accuracy of information against official health guidelines and the scientific literature.

A thematic analysis was conducted on 71 thread starts and 1,281 comments from Mumsnet. Data was collected via web scraping, followed by manual screening. Themes were identified, and information-sharing posts were fact-checked against scientific evidence and guidelines.

Two overarching themes with five sub-themes emerged: "Type of reassurance offered", where users offered reassurance to alleviate worries, and "Reactions to reassurance", where some users appeared reassured while others did not. While many found reassurance, fact-checking revealed that the majority of the information was inaccurate, often underestimating the risks of prenatal alcohol exposure.

Online forums may provide a source of peer support to those who have consumed alcohol before pregnancy awareness but frequently spread misinformation about alcohol use in early pregnancy. Health professionals should ensure pregnant women have access to accurate information alongside appropriate support to reduce anxiety and avoid the spread of harmful misinformation.

Prenatal alcohol exposure (PAE) impacts hippocampal structure and function, contributing to deficits in memory and decision-making in affected individuals. Here, we evaluate hippocampal anomalies in children with PAE and an unexposed comparison group using advanced MRI methods that characterize hippocampal curvature and thickness.

Participants, ages 8 to 16 years, included children with PAE (n = 48) and an unexposed comparison group (n = 46) who underwent a dysmorphology exam, neuropsychological assessment, and an MRI scan. Height, weight, head circumference, and dysmorphic facial features were evaluated. Of those with PAE, 4.2% had fetal alcohol syndrome (FAS), 22.9% had partial FAS, and 72.9% had alcohol-related neurodevelopmental disorder. Neuropsychological testing included measures of intelligence and memory functioning. T1-weighted anatomical data were processed with the Hippunfold pipeline, which "unfolds" the complex hippocampal structure onto a template surface and provides measures of thickness and gyrification/curvature at each vertex. Permutation Analysis of Linear Models (PALM) was used to test for group differences (PAE vs. comparison) in hippocampal thickness and gyrification at each vertex and also to assess correlations with cognitive functioning.

There were significant regional differences in thickness and gyrification across bilateral hippocampi, with the PAE group showing substantially thinner tissue and less curvature than the comparison group, especially in CA1 and subiculum regions. For those with PAE, thinner subicular tissue (bilateral) was associated with lower IQ. Also in the PAE group, lower episodic memory performance was associated with thinness in the right hippocampus, especially in the subiculum region. There were no significant regional hippocampal patterns that were associated with cognitive functioning for individuals in the unexposed comparison group.

We used a novel MRI method to evaluate hippocampal structure in children with PAE and an unexposed comparison group. The data suggest that PAE disrupts hippocampal development, impacting both the early-stage folding of the structure and its ultimate thickness. The data also demonstrate that these developmental anomalies have functional consequences in terms of core memory functions as well as global intellectual functioning in children with PAE.

Fetal alcohol spectrum disorder (FASD) refers to a range of conditions caused by prenatal exposure to alcohol. First described in the 1970s as fetal alcohol syndrome, continuing progress has been made in the understanding, recognition and treatment of what is now recognized to be a range of related neurodevelopmental disorders. FASD is common, especially in countries with higher levels of alcohol consumption such as those in Europe and North America, where the prevalence is estimated to be around 3%. A number of diagnostic systems are in operation in different countries, and work is ongoing to develop an internationally agreed set of diagnostic criteria. People with FASD often have other developmental, mental and somatic conditions, and there appears to be a high rate of traumatic and other adverse experiences in this population. People with FASD are at increased risk of being involved in the criminal justice system, but they may be ill-equipped to successfully navigate it and are likely to provide false confessions, leading to wrongful convictions. Some interventions and treatments have been shown to be effective in improving functioning in children and families affected by FASD, which tend to take the form of coaching, education, advocacy and support. People with FASD have many strengths, which are often overlooked in research. They have been described as skilled musicians, artists and sportspeople with wide vocabularies who are resilient, compassionate, hard-working, and kind. Increasing attention is being paid to FASD but this is not enough. More research, diagnostic capacity, recognition, understanding, infrastructure and support are needed across the world.

We sought to determine risk factors for fetal alcohol spectrum disorders (FASD) in the United States.

Mothers of first-grade children participating in the Collaboration on FASD Prevalence (CoFASP) in three regional sites were interviewed. Maternal and paternal data were reported by mothers of children with an FASD diagnosis and controls.

Interviews were conducted with mothers of children with an FASD (n = 114) and controls (n = 753). Fifty-seven percent of control mothers usually drank 2.7 drinks per drinking day (DDD) once per month prior to pregnancy, and 79% of mothers of children with FASD reported drinking 4.2 drinks 1-2 times per week. Mothers of children with alcohol-related neurodevelopmental disorder reported the most alcohol consumption overall: bingeing, drinking frequency, drinking in each trimester, and other drug use. Mothers of children with fetal alcohol syndrome (FAS) and partial FAS (PFAS) underreported consumption. Distal maternal risk factors were liver problems, depression, later pregnancy recognition and first prenatal visit, lower frequency of marriage, and lower spirituality. Postnatal risk indicators were low birthweight and gestational age. Regression analysis indicated that maternal reports of three DDD before pregnancy were associated with a diagnosis within the FASD continuum (p < 0.001, OR = 9.92). First-trimester exposure (p < 0.001, OR = 7.64) and all three trimesters (p < 0.001, OR = 7.77) were associated with a child's FASD diagnosis. An independent association was found between paternal DDD during pregnancy and FASD diagnoses (p = 0.002, OR = 1.08); but, once maternal drinking was a covariate, paternal influence was not significant. Stepwise models indicated that combined maternal alcohol use measures (p < 0.001, χ2 = 61.09), later pregnancy recognition (p = 0.032, χ2 = 4.58), later prenatal visits (p = 0.036, χ2 = 4.38), and depression in lifetime (p = 0.002, χ2 = 9.47) were significant FASD predictors. The final 10-step model explained 27.4% of the variance in FASD risk.

While multiple, significant maternal risk factors for FASD were identified, paternal drinking was not a statistically significant, independent risk factor.

Diagnostic accuracy is important in systems used to diagnose common disorders such as Fetal Alcohol Spectrum Disorder (FASD). Currently, no comprehensive study has examined rates of agreement between different diagnostic criteria for FASD. This study estimates the likelihood that a diagnosis of FASD using one set of diagnostic criteria will result in the same diagnosis when compared to different diagnostic criteria. A systematic review was conducted to identify articles reporting on the comparison of two or more diagnostic criteria for a diagnosis of FASD. Inclusion criteria required that the study present data that estimated agreement for a diagnosis of FASD or no-FASD between two or more FASD criteria using two-by-two tables or presented data that could be used to generate the tables. Meta-analyses with confidence intervals were included to demonstrate variability in the estimates. Standardized measures of agreement were assessed using the kappa statistic with 95% confidence intervals and the phi coefficient as a measure of correlation between binary outcomes. The search identified six studies reporting on eight different FASD diagnostic criteria. The studies compared agreement between 17 different pairings of the criteria. For individual children, agreement ranged from 53.7% to 91%. The agreement between the eight different diagnostic criteria ranged from 59.4% to 89.5%. The kappa statistic found that five associations had a kappa ranging from 0.6 to 0.8. This study illustrates that comparisons of multiple pairs of diagnostic criteria are likely to result in considerable variation in diagnoses of FASD for individual children and between different criteria. The lack of agreement between these commonly used systems is likely to affect clinical care and studies where diagnosis is a key variable. Large-scale multicenter research is needed to examine factors contributing to variation in diagnostic outcomes.

The present chapter summarizes the clinical and preclinical findings collected to date, showing the impact of developmental alcohol exposure on sleep physiology. Sleep is a complex physiological process that plays a pivotal role in maintaining overall health and well-being via its involvement in regulating physiological, cognitive, and emotional functions. Clinical studies consistently report a high prevalence of sleep disturbances in children and adolescents diagnosed with fetal alcohol spectrum disorders (FASDs), including short sleep duration, sleep anxiety, bedtime resistance, increased sleep fragmentation, and parasomnias. It is established that alcohol consumption during gestation impairs brain development, leading to structural and functional alterations that may affect sleep architecture. In addition, clinical investigations have found a significant correlation between sleep-wake cycle disruptions and cognitive impairments after developmental alcohol exposure, and sleep disturbances are increasingly recognized as a substantial problem among FASD patients. However, the molecular mechanisms underlying these disturbances are poorly understood. Surprisingly, few studies with animal models of FASDs have characterized the effect of developmental ethanol exposure on sleep physiology, and these have focused on high doses. This chapter provides an overview of the current knowledge, reports the sleep disturbances in FASD patients, and then summarizes the gap in understanding the molecular and physiological mechanisms.

Background/Objectives: Sleep disturbances are common among children with fetal alcohol spectrum disorders (FASD) and are often accompanied by emotional and behavioral challenges. This study aimed to evaluate the relationship between sleep problems, anxiety, and depressive symptoms in children with FASD. Methods: The study included 90 children aged 7 to 16 years diagnosed with FASD, who were primarily in foster or adoptive care. Participants completed validated psychometric tools, including the Children's Sleep Habits Questionnaire (CSHQ), State Trait Anxiety Inventory for Children (STAIC) and Children's Depression Inventory 2 (CDI 2). Results: Sleep disturbances were significant, with 71.1% of participants scoring above the clinical threshold in CSHQ. State anxiety, measured by STAIC C-1, was positively correlated with specific sleep difficulties, such as bedtime resistance (r = 0.30, p = 0.008) and sleep anxiety (r = 0.31, p = 0.005). However, no correlation was found between trait anxiety (STAIC C-2) and sleep problems. Parent-reported depressive symptoms, measured using CDI 2:P, were strongly associated with general sleep disturbances (r = 0.27, p < 0.011), parasomnias (r = 0.33, p = 0.002) and daytime sleepiness (r = 0.34, p < 0.001). Conclusions: These findings suggest that sleep disturbances in children with FASD are closely related to state anxiety and depressive symptoms. The results emphasize the need for targeted interventions addressing sleep and emotional health in this population. Further research is needed to examine these relationships and their implications for clinical practice.

Research has examined a range of impacts of women's drinking on children. However, fewer studies have addressed the consequences of men's heavy drinking on children. This review aims to identify and describe men's behaviours and actions that arise from their drinking and are likely to cause harm to children, and the types of harms that stem from men's drinking that children experience.

Review articles from 1990 to September 2023 were included. Four health and social databases were searched for reviews that included terms relating to men, alcohol consumption, and child harms. From 1,873 identified articles, 19 articles met the criteria for inclusion.

Four broad topics were identified: relationships and families; violence and maltreatment; health, psychological and wellbeing impacts; and social and educational outcomes for children. Children may experience both direct and indirect harms associated with men's drinking. The former includes examples where men's drinking was linked to disinhibition, aggression, and physical assault. In the latter, men were absent resulting in being emotionally unavailable due to drinking. Internalising and externalising behaviours were common outcomes for children exposed to men's drinking. Contextual factors such as poverty, cultural norms and patriarchal influences were interrelated and sometimes exacerbated harm to children from men's drinking.

This review highlights the immediate and longer-lasting consequences of men's drinking for children, including family conflict, maltreatment, and emotional distress. Future studies should address gender disparities and consider the social factors present in cases where children are exposed to men's drinking.

To quantify regional subcortical brain volume anomalies in youth with fetal alcohol spectrum disorder (FASD), assess the relative sensitivity and specificity of abnormal volumes in FASD vs. a comparison group, and examine associations with cognitive function.

Participants: 47 children with FASD and 39 typically-developing comparison participants, ages 8-17 years, who completed physical evaluations, cognitive and behavioral testing, and an MRI brain scan. A large normative MRI dataset that controlled for sex, age, and intracranial volume was used to quantify the developmental status of 7 bilateral subcortical regional volumes. Z-scores were calculated based on volumetric differences from the normative sample. T-tests compared subcortical volumes across groups. Percentages of atypical volumes are reported as are sensitivity and specificity in discriminating groups. Lastly, Pearson correlations examined the relationships between subcortical volumes and neurocognitive performance.

Participants with FASD demonstrated lower mean volumes across a majority of subcortical regions relative to the comparison group with prominent group differences in the bilateral hippocampi and bilateral caudate. More individuals with FASD (89%) had one or more abnormally small volume compared to 72% of the comparison group. The bilateral hippocampi, bilateral putamen, and right pallidum were most sensitive in discriminating those with FASD from the comparison group. Exploratory analyses revealed associations between subcortical volumes and cognitive functioning that differed across groups.

In this sample, youth with FASD had a greater number of atypically small subcortical volumes than individuals without FASD. Findings suggest MRI may have utility in identifying individuals with structural brain anomalies resulting from PAE.

Prenatal alcohol exposure (PAE) is associated with long-term neurodevelopmental deficits resulting in impaired executive functioning and motor control. Intriguingly, PAE has been linked with an increased risk of transient systemic hypoxia-ischemia (TSHI), which alone results in suboptimal fetal growth and neurodevelopmental consequences. Here, using two translationally relevant preclinical models, we investigated the short-term and lasting effects of PAE and TSHI on the morphology of the medial prefrontal cortex (mPFC), a region important in executive function, and tested whether PAE interacts with TSHI to produce a distinct pattern of injury relative to either condition alone. The four experimental groups included sham (saccharin water, no TSHI), PAE (5% alcohol, no TSHI), TSHI (saccharin water, TSHI), and PAE+TSHI (5% alcohol, TSHI). Brains were extracted for Golgi-Cox staining at Postnatal Day 35 (P35) or P100 and processed for 3D Sholl analysis. The analysis of the mPFC at P35 showed no significant differences in the number of branches or dendritic length overall, although the impact of TSHI compared to alcohol was significant for both. There were no significant differences in the number of Sholl intersections overall at P35, although a sex difference was noted in PAE offspring. At P100, analysis of filament dendritic length and branching number was also significantly impacted by TSHI compared to alcohol. Interestingly, sex was also a significant factor when assessing the impact of alcohol. PAE and TSHI both had an insignificantly increased number of Sholl intersections at P100 compared to the control. The observed changes to dendritic complexity at P100 demonstrate altered neuronal morphology in the mPFC that endure into adulthood. Given the importance of the mPFC in executive functioning, these pilot data provide insight into morphological changes that may contribute to the neurobehavioral deficits observed following exposure to PAE and TSHI and highlight the need for additional investigations into this area.

Fetal Alcohol Spectrum Disorder (FASD) encompasses the deleterious consequences of Prenatal Alcohol Exposure (PAE), including developmental delay, microcephaly, dysmorphologies, and cognitive and behavioral issues. The dose and timing of alcohol exposure, maternal and environmental factors, and genetics all impact FASD outcomes, but differential susceptibility and resiliency to PAE remains poorly understood. In this study, we examined the differential effects of PAE during early mouse development on brain growth and gene expression. Brains were weighed and collected either 24 hours or five days after treatment. We then performed transcriptomics to determine whether offspring differentially affected by PAE, by brain weight, also differ in gene expression, despite having the same genetic background, alcohol exposure, and maternal factors. We found within litter variation in brain weights after PAE, and classified offspring as having normal, middle, and low-weight brains relative to saline-treated controls. The normal-weight brains showed no significant differences in gene expression, suggesting these offspring were both phenotypically and transcriptionally unaffected by PAE. While both middle- and low-weight brains showed changes in gene expression, the middle-weight brains showed the most robust transcriptome differences. Twenty-four hours after PAE, we saw an upregulation of cell cycle and apoptosis in affected offspring, whereas at roughly a week later, we saw a downregulation of metabolic processes. Overall, these findings highlight variability in response to PAE and demonstrate the molecular processes involved in offspring phenotypically affected by alcohol.

Alcohol is a known teratogen and prenatal alcohol exposure remains a major ongoing public health concern. Fetal alcohol spectrum disorder has become the diagnosis for describing individuals who have been affected by prenatal alcohol exposure. In this Viewpoint, we raise major concerns about its continued use as a diagnostic term in how it perpetuates a misleading and outdated narrative about child development and maternal health. We argue that the term fetal alcohol spectrum disorder has contributed to a culture of racism and discrimination for many who are diagnosed with it. The term fetal alcohol spectrum disorder fails to capture the progress made in our collective understanding of neurodevelopment through advancements in the field of genetics and in understanding the effects of trauma and adversity. We call for urgent international collaborative action to review the use of it as a diagnostic term and, more broadly, to reconsider the practice of diagnosing disabilities as medical illnesses. We suggest that this practice fails to recognise that outcomes of functioning and participation in individuals are not only the results of health conditions, but are also the products of complex interactions and experiences of individuals within the families and societies in which they live.

Fetal Alcohol Spectrum Disorder (FASD) is a lifelong disorder caused by prenatal alcohol exposure (PAE) and is one of the most common causes of brain damage and developmental disability. FASD has been characterized by an array of symptoms that negatively affects cognitive, social, and adaptive functioning. Individuals living with FASD, relative to the general population, are more likely to become entangled in the legal system due to challenges associated with the disorder. Moreover, symptomology of FASD often contributes to these individuals struggling in successfully navigating various stages of the legal system, including arrest, interrogation, working with their defense counsel, and courtroom appearances. The difficulties faced by defendants living with FASD are exacerbated by systemic failure from legal professionals in recognizing and accommodating for the extent and complexities of this disorder. Consequently, defendants living with FASD often do not receive effective due process of law in comparison to their neurotypical peers. Moreover, attempts at punishment and deterrence through probation and jail terms are often ineffective for individuals living with FASD because of the effects of their disorder. This article is intended to provide valuable information and best practices for professionals in the legal system, particularly judges, prosecutors, defense attorneys, social workers/mitigation specialists, and psychologists, who are likely to encounter individuals living with FASD or suspected FASD early in the judicial process.

Despite the recognized link between prenatal alcohol consumption and various congenital anomalies, the negative consequences for women's own health and family health, as well as the work done in healthcare to prevent alcohol in pregnancy, the acceptance of alcohol use during pregnancy persists in numerous communities around the world. Knowledge about women's alcohol use in pregnancy and how it relates to the social and cultural context they are part of is important to help and support women in abstaining during pregnancy. This meta-ethnography aims to offer a novel interpretation and conceptual understanding of the experiences of women who consume alcohol during pregnancy by synthesizing insights from existing qualitative studies.

An interpretative meta-ethnographic design was chosen based on a systematic literature search in seven electronic databases, and manual searches were conducted in 2023. The CASP checklist was used to assess the 18 included articles.

In the synthesis, we use the metaphor of being trapped in a maze to illustrate the complexity of pregnant women's experiences of drinking during pregnancy. Women who drink alcohol during pregnancy are navigating the maze in a whirlwind of conflicting information and knowledge. The findings show how sociocultural norms form rigid pathways within the maze. In relation to their sociocultural context, women use several motives to justify the routes chosen within the maze. The competing information, knowledge and clashing norms within women's sociocultural contexts leave women to navigate alone in the maze.

Alcohol in pregnancy needs to be conceptualized as an issue positioned at the intersection of social sciences and healthcare and needs to be handled accordingly, both through transdisciplinary research, by early prevention and multimodal interventions in healthcare and the broader society. Such interventions would benefit from drawing on knowledge about women's experiences with alcohol in pregnancy.

Fetal alcohol spectrum disorder (FASD) is a significant public health concern, yet there is no internationally agreed set of diagnostic criteria or summary of underlying evidence to inform diagnostic decision-making. This systematic review assesses associations of prenatal alcohol exposure (PAE) and outcomes of diagnostic assessments, providing an evidence base for the improvement of FASD diagnostic criteria.

Six databases were searched (inception-February 2023). Case-controls or cohort studies examining associations between participants with/without PAE or a FASD diagnosis and the domains of physical size, dysmorphology, functional neurodevelopment and/or brain structure/neurology were included. Excluded studies were non-empirical, sample size < 10, PAE determined via biological markers only, or no suitable comparison group. Summary data were extracted and associations between outcomes and standardised levels of PAE or FASD diagnosis determined using random-effects meta-analyses. Certainty of the evidence was assessed using GRADE.

Of the 306 included studies, 106 reported physical size, 43 dysmorphology, 195 functional neurodevelopment and 110 structural/neurological outcomes, with 292 different outcomes examined. There was a dose-response relationship between PAE and head circumference, as well as measures of physical size, particularly at birth. There was also an association between higher PAE levels and characteristic sentinel facial dysmorphology, as well as many of the current functional neurodevelopmental outcomes considered during diagnosis. However, data were often lacking across the full range of exposures. There was a lack of evidence from studies examining PAE to support inclusion of non-sentinel dysmorphic features, social cognition, speech-sound impairments, neurological conditions, seizures, sensory processing or structural brain abnormalities (via clinical MRI) in diagnostic criteria. GRADE ratings ranged from very low to moderate certainty of evidence.

This comprehensive review provides guidance on which components are most useful to consider in the diagnostic criteria for FASD. It also highlights numerous gaps in the available evidence. Future well-designed pregnancy cohort studies should specifically focus on dose-response relationships between PAE and dysmorphology, neurodevelopment and brain structure/neurological outcomes.

PROSPERO: CRD42021230522.

Malnutrition is a significant concern in paediatric populations, particularly among children with neurodevelopmental disorders such as foetal alcohol spectrum disorder (FASD). This study aimed to examine macronutrient and micronutrient imbalances and assess the nutritional status of a group of patients with FASD.

This study involved an analysis of the serum levels of key nutrients in a group of children diagnosed with FASD. Macronutrients and micronutrients were measured to identify any imbalances, including vitamin D, B12, E, A, albumin, and serum protein, among others.

The study found a high prevalence of vitamin D deficiency among the patients. Additionally, elevated serum concentrations of micronutrients such as vitamin B12, E, and A were observed in 8%, 7%, and 19% of patients, respectively. Macronutrient imbalances were noted, including high levels of albumin and serum protein, indicating a possible metabolic disturbance. Unexpectedly, high rates of hypercholesterolemia were observed, raising concerns about an increased risk of metabolic syndrome in this population.

These findings suggest that the principal issue among patients with FASD is an altered metabolism rather than nutritional deficiencies. Potential causes of these abnormalities could include oxidative stress and changes in body composition. The results underline the need for further research to better understand the unique nutritional challenges in children with FASD and to guide the development of targeted therapeutic strategies.

Fetal alcohol spectrum disorder (FASD) is a leading cause of neurodevelopmental disability globally. International organizations have highlighted an urgent need for improved prevention, diagnosis, and support. However, the evidence base needed to inform this is thought to be limited. We conducted two complementary reviews to (i) describe trends in the volume and characteristics of original FASD research articles (Review 1) and (ii) compare the volume of published research on FASD to that of other neurodevelopmental disorders (Review 2). In Review 1, we systematically searched MEDLINE, Embase, CINAHL and PsycInfo for original studies with FASD terms in the title, published between 2000 and 2023. We summarised study characteristics including the article topic(s), sample population, country of origin, and publication year using quantitative content analysis and time-series plots. A total of 854 studies were eligible. Studies showed a relative focus on diagnosis and screening, compared to prevention and intervention. FASD research originated from 31 countries, however most countries (68%) had fewer than 10 articles published over the 23-year review period. In Review 2, we searched PubMed for records published between 2000 and 2023 with FASD, autism, or attention-deficit-hyperactivity disorder (ADHD) terms in the title. We compared the volume of records for these conditions using descriptive statistics and time-series plots. Of the 64,069 records retrieved, 2% were for FASD, compared to 60% for autism and 38% for ADHD. FASD remains considerably under-researched. While there has been an increase in the number of original FASD research articles published annually over time, this is much lower than expected compared to publication trends for other neurodevelopmental conditions, and the wider scientific literature. Further research is needed to understand the impact of FASD across the lifespan, to inform evidence-based policy and support, and to advance progress in strength-based, stigma-reducing approaches to FASD research and practice.

During pregnancy, exposure to alcohol represents an environmental insult capable of negatively impacting embryonic development. This influence can stem from disruption of molecular profiles, ultimately leading to manifestation of fetal alcohol spectrum disorder. Despite the central role of the placenta in proper embryonic development and successful pregnancy, studies on the placenta in a prenatal alcohol exposure and fetal alcohol spectrum disorder context are markedly lacking. Here, we employed a well-established model for preimplantation alcohol exposure, specifically targeting embryonic day 2.5, corresponding to the 8-cell stage. The exposure was administered to pregnant C57BL/6 female mice through subcutaneous injection, involving two doses of either 2.5 g/kg 50 % ethanol or an equivalent volume of saline at 2-hour intervals. Morphology, DNA methylation and gene expression patterns were assessed in male and female late-gestation (E18.5) placentas. While overall placental morphology was not altered, we found a significant decrease in male ethanol-exposed embryo weights. When looking at molecular profiles, we uncovered numerous differentially methylated regions (DMRs; 991 in males; 1309 in females) and differentially expressed genes (DEGs; 1046 in males; 340 in females) in the placentas. Remarkably, only 21 DMRs and 54 DEGs were common to both sexes, which were enriched for genes involved in growth factor response pathways. Preimplantation alcohol exposure had a greater impact on imprinted genes expression in male placentas (imprinted DEGs: 18 in males; 1 in females). Finally, by using machine learning model (L1 regularization), we were able to precisely discriminate control and ethanol-exposed placentas based on their specific DNA methylation patterns. This is the first study demonstrating that preimplantation alcohol exposure alters the DNA methylation and transcriptomic profiles of late-gestation placentas in a sex-specific manner. Our findings highlight that the DNA methylation profiles of the placenta could serve as a potent predictive molecular signature for early preimplantation alcohol exposure.

Exposure to alcohol and/or other addictive drugs in pregnancy is a documented risk factor for neurological impairment. We aimed to assess neurodevelopmental outcome at two years of age in infants exposed to prenatal alcohol and/or other addictive drugs and to examine the predictive value of early motor assessment.

This was a follow-up at two years of age in the prospective cohort study Children Exposed to Alcohol and/or Drugs in Intrauterine Life (CEADIL). The exposed group comprised 73 infants recruited from primary health care and included in a hospital follow-up programme at St. Olavs Hospital, Trondheim University Hospital, Norway. The control group comprised 93 healthy, unexposed infants recruited from the maternity ward at the same hospital. All children had been assessed by physiotherapists using the General Movement Assessment (GMA) at three months of age. Presence of fidgety movements, movement character and the Motor Optimality Score - Revised (MOS-R) were used. At two years of age, the children were assessed by trained examiners using the Bayley Scales of Infant and Toddler Development - Third Edition (BSID-III), Ages & Stages Questionnaires: Social-Emotional (ASQ:SE) and the Hollingshead Two-Factor Index of Social Position (SES).

The cognitive, language and motor composite scores of BSID-III were considerably lower in the exposed group than in the control group. Mean differences adjusted for age and parental SES ranged from - 13.3 (95% confidence interval, CI: -18.6 to -8.0) to -17.7 (95% CI: -23.3 to -12.2). Suboptimal fidgety movements and monotonous movement character had high sensitivity (0.94 to 0.74), but low specificity (0.10 to 0.32), while sensitivity and specificity of the MOS-R was around 50 and 60%, respectively.

Neurodevelopmental outcome at two years of age was poorer in a group of children exposed to alcohol and/or drugs in pregnancy compared with a control group of healthy, unexposed children. Sensitivity of suboptimal fidgety movements and monotonous movement character at three months of age for later neurodevelopmental outcome was high to acceptable, but the MOS-R had limited sensitivity.

Fetal Alcohol Spectrum Disorder (FASD) is one of the leading non-genetic causes of developmental disability worldwide and is thought to be particularly common in the UK. Despite this, there is a lack of data on FASD in the UK.

To conduct public and professional involvement work to establish stakeholder views on the feasibility, acceptability, key purposes, and design of a national linked longitudinal research database for FASD in the UK.

We consulted with stakeholders using online workshops (one for adults with FASD [and their supporters] N = 5; one for caregivers of people with FASD (N=7), 1:1/small-team video calls/email communication with clinicians, policymakers, data-governance experts, third-sector representatives, and researchers [N=35]), and one hybrid clinical workshop (N = 17). Discussions covered data availability, benefits, challenges, and design preferences for a national pseudonymised linked database for FASD. We derived key themes from the notes and recordings collected across all involvement activities.

Our tailored, multi-method approach generated high levels of stakeholder engagement. Stakeholders expressed support for a pseudonymised national linked database for FASD. Key anticipated benefits were the potential for: increased awareness and understanding of FASD leading to better support; new insights into clinical profiles leading to greater diagnostic efficiency; facilitating international collaboration; and increased knowledge of the long-term impacts of FASD on health, social care, education, economic and criminal justice outcomes. Given the rich data infrastructure established in the UK, stakeholders expressed that a national linked FASD database could be world-leading. Common stakeholder concerns were around privacy and data-sharing and the importance of retaining space for clinical judgement alongside insights gained from quantitative analyses.

Multi-method and multidisciplinary public and professional involvement activities demonstrated support for a national linked database for FASD in the UK. Flexible, diverse, embedded stakeholder collaboration will be essential as we establish this database.

Studies of youth and young adults with prenatal alcohol exposure (PAE) have most consistently reported reduced volumes of the corpus callosum, cerebellum and subcortical structures. However, it is unknown whether this continues into middle adulthood or if individuals with PAE may experience premature volumetric decline with aging. Forty-eight individuals with fetal alcohol spectrum disorders (FASD) and 28 healthy comparison participants aged 30 to 65 participated in a 3T MRI session that resulted in usable T1-weighted and T2-weighted structural images. Primary analyses included volumetric measurements of the caudate, putamen, pallidum, cerebellum and corpus callosum using FreeSurfer software. Analyses were conducted examining both raw volumetric measurements and subcortical volumes adjusted for overall intracranial volume (ICV). Models tested for main effects of age, sex and group, as well as interactions of group with age and group with sex. We found the main effects for group; all regions were significantly smaller in participants with FASD for models using raw volumes (P's < 0.001) as well as for models using volumes adjusted for ICV (P's < 0.046). Although there were no significant interactions of group with age, females with FASD had smaller corpus callosum volumes relative to both healthy comparison females and males with FASD (P's < 0.001). As seen in children and adolescents, adults aged 30 to 65 with FASD showed reduced volumes of subcortical structures relative to healthy comparison adults, suggesting persistent impact of PAE. Moreover, the observed volumetric reduction of the corpus callosum in females with FASD could suggest more rapid degeneration, which may have implications for cognition as these individuals continue to age.

Background: Fetal Alcohol Spectrum Disorder (FASD) is a common neurodevelopmental disorder but may be underrecognized and misunderstood by people who provide health and social support services. The aim of the research is to understand the FASD knowledge, attitudes, and practices among people employed by the social and community sector in New Zealand. Methods: We conducted an online survey of people working in the New Zealand social and community sector (i.e., social workers, support workers). The survey focused on the following areas: awareness of FASD; knowledge and beliefs about FASD; the impact of FASD on professional practice; and training needs. Results: Most participants reported a basic understanding of FASD, however only 5% felt very well prepared to support someone with FASD. A large majority of participants believed that FASD diagnosis may be stigmatising for individuals or families. Conclusion: There is a need to improve training, professional development, and workplace support for social and community workers in New Zealand to support people with FASD.