<h4>Background</h4>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.<h4>Methods</h4>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.<h4>Results</h4>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 ran
Fetal alcohol spectrum disorder (FASD) is the leading cause of non-genetic developmental disability in many countries, affecting an estimated 7.7 per 1000 individuals [ 1 ]. Consequently, FASD is a serious public health issue, associated with significant costs for the individual, family and society [ 2 ]. FASD is under-diagnosed globally, in part owing to the current lack of a unified diagnostic approach [ 3 ]. Due to the complex and heterogeneous nature of FASD, over ten different diagnostic criteria are currently employed internationally [ 4 ].
Where multiple study PAE categories were classified into the same exposure level defined in this review, the higher PAE category from the study was used in the analyses. Example calculations for standardising PAE levels are provided in Additional file 1: Table S5. Standardisation of diagnostic categories For diagnosed studies, four categories were used to group diagnoses: FASD, FAS (fetal alcohol syndrome), pFAS (partial fetal alcohol syndrome) and ARND/other (alcohol-related neurodevelopmental disorder). FASD was used when a study grouped all individuals with an FASD diagnostic outcome together.
Association between prenatal alcohol exposure (PAE) or fetal alcohol spectrum disorder (FASD) diagnosis and academic achievement. Fig. S18. Association between prenatal alcohol exposure (PAE) and general intellectual abilities (sub-scales). Fig. S19. Association between fetal alcohol spectrum disorder (FASD) diagnoses and general intellectual abilities. Fig. S20. Association between prenatal alcohol exposure (PAE) or fetal alcohol spectrum disorder (FASD) diagnosis and measures of memory. Fig. S21. Association between prenatal alcohol exposure (PAE) and adaptive and social behaviour. Fig. S22.
Association between Fetal Alcohol Spectrum Disorder (FASD) and quantitative magnetic resonance imaging (MRI) measures. Fig. S28. Association between prenatal alcohol exposure (PAE) or fetal alcohol syndrome (FAS) diagnosis and other neurological outcomes.
Association between prenatal alcohol exposure (PAE) or fetal alcohol spectrum disorder (FASD) diagnosis and sentinel facial features. Fig. S5. Association between prenatal alcohol exposure (PAE) and minor dysmorphology features. Fig. S6. Association between fetal alcohol spectrum disorder (FASD) diagnoses and minor dysmorphology features. Fig. S7. Association between prenatal alcohol exposure (PAE) or fetal alcohol spectrum disorder (FASD) diagnosis and dysmorphology scores. Fig. S8. Association between prenatal alcohol exposure (PAE) or fetal alcohol spectrum disorder (FASD) diagnosis and measures of attention. Fig. S9.
Association between fetal alcohol spectrum disorder (FASD) diagnosis and direct measures of executive functioning. Fig. S10. Association between prenatal alcohol exposure
Association between prenatal alcohol exposure (PAE) or fetal alcohol spectrum disorder (FASD) diagnosis and measures of memory. Fig. S21. Association between prenatal alcohol exposure (PAE) and adaptive and social behaviour. Fig. S22. Association between fetal alcohol spectrum disorder (FASD) diagnosis and adaptive and social behaviour. Fig. S23. Association between prenatal alcohol exposure (PAE) or fetal alcohol spectrum disorder (FASD) diagnosis and sensory processing/neurological signs. Fig. S24. Association between fetal alcohol spectrum disorder (FASD) diagnosis and head circumference. Fig. S25.
Association between prenatal alcohol exposure (PAE) or fetal alcohol spectrum disorder (FASD) diagnosis and structural brain abnormalities from clinical magnetic resonance imaging (MRI). Fig. S26. Association between prenatal alcohol exposure (PAE) and quantitative magnetic resonance imaging (MRI). Fig. S27. Association between Fetal Alcohol Spectrum Disorder (FASD) and quantitative magnetic resonance imaging (MRI) measures. Fig. S28. Association between prenatal alcohol exposure (PAE) or fetal alcohol syndrome (FAS) diagnosis and other neurological outcomes.
Introduction One of the most sensitive disabilities in human beings is intellectual disability. In April, 2003, a 10-month study was completed of all persons in Cuba with mental retardation (MR), producing results that included epidemiological variables on a national scale. Objective Through follow-up research, this paper describes and analyzes 4 prenatal factors associated with MR: Down syndrome (DS), fragile X syndrome (FXS), consanguinity, and maternal alcohol use during pregnancy, in order to provide recommendations for health system decision-makers on consolidating prevention strategies at the community level and improving individual attention to persons with MR. Materials & Methods All studies were carried out on the basis of strict ethical principles. Data for the 4 prenatal factors was gleaned from the national study's database. Additional data on affected individuals was obtained through home visits. A previously developed screening instrument was used for clinical genetic analysis to classify possible MR causal factors as prenatal, perinatal, postnatal, psychosis, and unclassifiable. Prenatal included causal factors such as: genetic (by clinical genetic examination, metabolic screening in urine, and routine karyotypes); nonspecific (evidence of prenatal causal factor without diagnosis of genetic or environmental etiology); and environmental (prenatal medical history of biological, physical, or chemical teratogens, endocrine-metabolic diseases, or other maternal diseases known to affect fetal neurodevelopment). Frequency, prevalence, and percentages were reported using a descriptive statistical method. Impact of interventions and actions over time were also compared. Results MR prevalence in Cuba is 1.25%, lower than the value of 2%-3% reported in developed countries. National prevalence of DS was found to be 4.3 per 10,000 population, representing 22.1% of persons with MR attributed to an ascertained genetic cause. FXS prevalence in a population of individuals of both sexes with MR, initially classified as nonspecific prenatal, psychosis, and unclassifiable, was 2.5 per 1,000 of that population; however, in males of the same population, prevalence was 3.7 per 1,000. At this first stage, such results indicate that this syndrome contributes biologically to the 1.46:1 male/female ratio among the 140,489 individuals with MR. Maternal alcohol use during pregnancy was found in 4.22% of persons with MR and consanguinity was present in 6.89% of the population with MR (10.9% of persons with mild prenatal MR and 14.2% with severe MR). This national data is subdivided by regions and provinces in this paper. Conclusions Prevalence of MR in Cuba is lower than reference values for developed countries. Knowledge generated by this study about 4 specific causes of MR constitutes pioneering research in the Cuban context, contributing to the field of medical genetics. The results offer the basis for formulation of new scientific contributions related to MR genetics as well as preventive approaches to such genetic factors as consanguinity and to environmental factors such as maternal alcohol use during pregnancy, which affect or target embryo-fetal development of the nervous system.
<i>Background:</i> Ethanol consumption during pregnancy induces enduring detrimental effects in the offspring, manifesting as a spectrum of symptoms collectively termed as Fetal Alcohol Spectrum Disorders (FASD). Presently, there is a scarcity of treatments for FASD.<i>Objectives:</i> To analyze current literature, emphasizing evidence derived from preclinical models, that could potentially inform therapeutic interventions for FASD.<i>Methods:</i> A narrative review was conducted focusing on four prospective treatments: nutritional supplements, antioxidants, anti-inflammatory compounds and environmental enrichment. The review also highlights innovative therapeutic strategies applied during early (e.g. folate administration, postnatal days 4-9) or late (e.g. NOX2 inhibitors given after weaning) postnatal stages that resulted in significant improvements in behavioral responses during adolescence (a critical period marked by the emergence of mental health issues in humans).<i>Results:</i> Our findings underscore the value of treatments centered around nutritional supplementation or environmental enrichment, aimed at mitigating oxidative stress and inflammation, implying shared mechanisms in FASD pathogenesis. Moreover, the review spotlights emerging evidence pertaining to the involvement of novel molecular components with potential pharmacological targets (such as NOX2, MCP1/CCR2, PPARJ, and PDE1).<i>Conclusions:</i> Preclinical studies have identified oxidative imbalance and neuroinflammation as relevant pathological mechanisms induced by prenatal ethanol exposure. The relevance of these mechanisms, which exhibit positive feedback loop mechanisms, appear to peak during early development and decreases in adulthood. These findings provide a framework for the future development of therapeutic avenues in the development of specific clinical treatments for FASD.
<h4>Purpose</h4>To describe allied health and educational interventions and their effectiveness for children and adolescents with fetal alcohol spectrum disorder (FASD). To appraise the quality and strength of studies.<h4>Methods</h4>Electronic databases were searched between 2005 and March 2022, identifying non-pharmacological studies supporting function, activity, or participation for FASD participants aged 5-18 years using any quantitative research design. Outcomes were coded using International Classification of Functioning, Disability and Health, family of Participation Related Constructs and behaviour categories. Multi-level random-effects meta-analysis examined intervention effects. Study methodological quality was evaluated using Cochrane risk of bias tools, RoBiNT, AMSTAR 2 and NHMRC Hierarchy levels of evidence. Certainty of findings were synthesised using GRADE approach.<h4>Results</h4>The systematic review included 25 studies with 735 participants, 10 of which were analysed by meta-analysis. Body function and structure, activity, behaviour, and sense of self outcomes were pooled. A small, positive effect favouring interventions was found (<i>g</i> = 0.29, 95% CI = 0.15-0.43), however the GRADE certainty was rated as low. No participation outcomes were identified.<h4>Conclusions</h4>Some interventions targeting body function and structure, activity and behaviour outcomes were effective. Evidence of interventions that support children's and adolescent's participation as an outcome is lacking.
<b>Purpose:</b> Fetal alcohol syndrome (FAS) results from the teratogenic effects of alcohol on the fetus. Oral manifestations are commonly found in FAS and contribute to the diagnosis. The purpose of this study was to provide a review of the literature and describe two cases of FAS.<br/><b>Methods:</b> Electronic searches were conducted in August 2021 in multiple databases. The cases of two children with FAS are reported.<br/><b>Results:</b> One hundred sixty-six articles were included. The oral features frequently reported were micrognathia, cleft palate, high arched palate, maxillary hypoplasia, prognathia and crowding. The first patient had systemic and orofacial changes, such as delayed physical and cognitive development, micrognathia, tooth impaction, malocclusion and enamel hypoplasia. The second child had cognitive, and speech and behavioral deficits, but no oral and dental abnormalities.<br/><b>Conclusion:</b> Dentists should be aware of clinical findings since they may take part in the diagnosis and management of FAS.
The adverse effects of prenatal alcohol exposure constitute a continuum of disabilities (fetal alcohol spectrum disorders [FASD]). In 1996, the Institute of Medicine established diagnostic categories delineating the spectrum but not specifying clinical criteria by which diagnoses could be assigned. In 2005, the authors published practical guidelines operationalizing the Institute of Medicine categories, allowing for standardization of FASD diagnoses in clinical settings. The purpose of the current report is to present updated diagnostic guidelines based on a thorough review of the literature and the authors' combined expertise based on the evaluation of >10 000 children for potential FASD in clinical settings and in epidemiologic studies in conjunction with National Institute on Alcohol Abuse and Alcoholism-funded studies, the Collaborative Initiative on Fetal Alcohol Spectrum Disorders, and the Collaboration on FASD Prevalence. The guidelines were formulated through conference calls and meetings held at National Institute on Alcohol Abuse and Alcoholism offices in Rockville, MD. Specific areas addressed include the following: precise definition of documented prenatal alcohol exposure; neurobehavioral criteria for diagnosis of fetal alcohol syndrome, partial fetal alcohol syndrome, and alcohol-related neurodevelopmental disorder; revised diagnostic criteria for alcohol-related birth defects; an updated comprehensive research dysmorphology scoring system; and a new lip/philtrum guide for the white population, incorporating a 45-degree view. The guidelines reflect consensus among a large and experienced cadre of FASD investigators in the fields of dysmorphology, epidemiology, neurology, psychology, developmental/behavioral pediatrics, and educational diagnostics. Their improved clarity and specificity will guide clinicians in accurate diagnosis of infants and children prenatally exposed to alcohol.
In utero alcohol exposure can disrupt the development of the fetal brain and result in a wide range of neurobehavioral outcomes collectively known as fetal alcohol spectrum disorders (FASD). This paper provides a comprehensive review of the cognitive and behavioral outcomes of prenatal alcohol exposure, including domains of general intelligence, executive functioning, language development, learning and memory, adaptive functioning, academic performance, and concurrent psychopathology. In addition, the current status of the neurobehavioral profile of FASD and its potential as a diagnostic tool will be discussed.
<h4>Background</h4>Sleep disturbances are prevalent in children with prenatal alcohol exposure (PAE), including those with Fetal Alcohol Spectrum Disorders (FASD), potentially exacerbating behavioural and cognitive deficits. Despite this, no review has systematically assessed the timing or severity of these sleep disturbances. The aim of this review was to identify sleep disturbances in children with PAE.<h4>Methods</h4>A systematic search across seven databases followed PRISMA guidelines. Studies included children aged 3-10 with PAE and provided quantitative sleep data. Two reviewers independently screened articles. A meta-analysis of subjective sleep outcomes used a random-effects model, with heterogeneity assessed via I<sup>2</sup>.<h4>Results</h4>Fourteen studies met inclusion criteria. Children with PAE had consistently worse sleep than typically developing peers, including longer sleep onset, shorter duration, more awakenings, lower sleep efficiency, and greater sleep variability. Higher PAE levels were linked to earlier onset and persistence of sleep disturbances, with more severe issues in early pregnancy exposure. Meta-analysis of seven studies showed high heterogeneity (I<sup>2</sup> = 0.91) with medium to large effect sizes, particularly for night awakenings (d = 1.04) and sleep duration (d = 0.89).<h4>Conclusions</h4>Children with PAE face persistent sleep disturbances, worsening with heavier or earlier exposure, highlighting the need for early screening and interventions.
<b>Background/objectives:</b> Alcohol use during pregnancy can result in adverse outcomes for the offspring, including Fetal Alcohol Spectrum Disorders (FASD). Psychosocial and contextual factors may influence gestational alcohol intake and women's risk perception. This systematic review aimed to assess pregnant women's and women of childbearing age's perceived risk of alcohol use during pregnancy and to evaluate their knowledge of its potential effects on children. <b>Methods:</b> Following the PRISMA guidelines, a systematic search was conducted in Web of Science, PubMed and PsycArticles databases for studies published up to May 2025. Eligible studies examined gestational alcohol use, risk perception, or knowledge of fetal consequences among pregnant women or women of reproductive age. Methodological quality was assessed with the Critical Appraisal of Qualitative Studies tool from the Centre for Evidence-Based Medicine (CEBM). <b>Results:</b> Twenty-nine studies were included. Reported prevalence of alcohol consumption during pregnancy varied considerably across settings. A substantial proportion of women perceived alcohol use during pregnancy as acceptable, often depending on quantity, frequency, type of beverage, or stage of gestation. Knowledge of FASDs was generally limited and frequently restricted to physical malformations. Misconceptions were more common among women with prior alcohol use. The findings highlight persistent gaps in risk perception and knowledge about FASDs. <b>Conclusions:</b> Prevention strategies should not be limited to pregnant women but should also target women of childbearing age, especially those with active drinking patterns, as well as their immediate sociocultural environment. Strengthening professional training, community-based interventions, and consistent public health messaging are essential to reduce gestational alcohol exposure.
<h4>Purpose</h4>This systematic review aims to investigate craniofacial symptoms, oral healthcare requirements, and management approaches for children diagnosed with Fetal Alcohol Spectrum Disorder (FASD).<h4>Methods</h4>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.<h4>Results</h4>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.<h4>Conclusion</h4>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.
The fetal alcohol syndrome is the third most common recognizable cause of mental retardation in the United States. Many of the features of the fetal alcohol syndrome are secondary to the effect of alcohol on brain development. These include microcephaly, short palpebral fissures, the long smooth philtrum and thin vermilion of the upper lip, joint anomalies, altered palmar crease pattern, and mental retardation. Approximately 40% of babies born to alcoholic women and 11% of babies born to nonalcoholic moderately drinking women have evidence of the prenatal effect of alcohol. Alcohol, like other teratogens, causes a spectrum of defects. Thus, affected children may show great variability from the fullblown fetal alcohol syndrome to much milder effects of alcohol, some of which may not be obvious until school age. A "safe" amount of alcohol probably does not exist for the pregnant woman. Depending on unknown factors, what may be a "safe" amount for some women, may be devastating to the unborn baby of another. Two factors, the severity of the maternal alcoholism and the extent and severity of the pattern of malformation, seem to be most predictive of the ultimate prognosis for children with the fetal alcohol syndrome. Any decision to file child abuse changes against a mother whose baby was prenatally exposed to alcohol should be based on the parents ability to provide a stable home environment and not on whether the baby has features of the fetal alcohol syndrome. The fetal alcoho
Everything we examined (12)
This check searched the claim as stated. It did not run a separate search for evidence against it.