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PubMed2007

Reprogramming of genetic networks during initiation of the Fetal Alcohol Syndrome.

Fetal Alcohol Spectrum Disorders (FASD) are birth defects that result from maternal alcohol use. We used a non a priori approach to prioritize candidate pathways during alcohol-induced teratogenicity in early mouse embryos. Two C57BL/6 substrains (B6J, B6N) served as the basis for study. Dosing pregnant dams with alcohol (2x 2.9 g/kg ethanol spaced 4 hr on day 8) induced FASD in B6J at a higher incidence than B6N embryos. Counter-exposure to PK11195 (4 mg/kg) significantly protected B6J embryos but slightly promoted FASD in B6N embryos. Microarray transcript profiling was performed on the embryonic headfold 3 hr after the first maternal alcohol injection (GEO data series accession GSE1074). This analysis revealed metabolic and cellular reprogramming that was substrain-specific and/or PK11195-dependent. Mapping ethanol-responsive KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways revealed down-regulation of ribosomal proteins and proteasome, and up-regulation of glycolysis and pentose phosphate pathway in B6N embryos; and significant up-regulation of tight junction, focal adhesion, adherens junction, and regulation of the actin cytoskeleton (and near-significant up-regulation of Wnt signaling and apoptosis) pathways in both substrains. Expression networks constructed computationally from these altered genes identified entry points for EtOH at several hubs (MAPK1, ALDH3A2, CD14, PFKM, TNFRSF1A, RPS6, IGF1, EGFR, PTEN) and for PK11195 at AKT1. Our findings are consistent with the growing view that developmental exposure to alcohol alters common signaling pathways linking receptor activation to cytoskeletal reorganization. The programmatic shift in cell motility and metabolic capacity further implies cell signals and responses that are integrated by the mitochondrial recognition site for PK11195.

Analysis of Variance↗
PubMed2005

[Alcohol and pregnancy].

Alcohol abuse in pregnancy causes fetal alcohol spectrum disorders ranging from discreet developmental problems to fetal alcohol syndrome. That is why pregnant women and the women considering pregnancy should abstain from alcohol. Fetal alcohol spectrum disorders occur even after drinking at early stages of pregnancy when women are not aware of being pregnant. According to one study 75% Czech women drank alcohol before pregnancy and one third of them continued during first three months of pregnancy. According to new epidemiological data 83.4% of Czech women aged between 18 and 40 drank alcohol during the year preceeding the pregnancy. The prevention in this area in the Czech Republic is clearly not satisfactory, and it is complicated by the alcohol advertising targeted at women, low taxation of alcohol and other factors.

Adolescent↗
PubMed2006

Pediatricians' knowledge, training, and experience in the care of children with fetal alcohol syndrome.

OBJECTIVES: Prenatal exposure to alcohol interferes with fetal development and is the leading preventable cause of birth defects and developmental disabilities. The purpose of this study was to identify current knowledge, diagnosis, prevention, and intervention practices related to fetal alcohol syndrome and related conditions by members of the American Academy of Pediatrics. METHODS: This study was developed collaboratively by the American Academy of Pediatrics and the Centers for Disease Control and Prevention. Questionnaires were mailed to a 3% random sample (n = 1600) of American Academy of Pediatrics members in the United States. General pediatricians, pediatric subspecialists, and pediatric residents were included. RESULTS: Participation rate was 55% (n = 879). Respondents almost universally knew the teratology and clinical presentation of fetal alcohol spectrum disorders. However, they were less likely to report comfort with routine pediatric care of these children. Whereas 62% felt prepared to identify and 50% felt prepared to diagnose, only 34% felt prepared to manage and coordinate the treatment of children with fetal alcohol spectrum disorders. Even fewer (n = 114 [13%]) reported that they routinely counsel adolescent patients about the risks of drinking and pregnancy. CONCLUSIONS: The survey confirms that pediatricians are knowledgeable about fetal alcohol syndrome but do not feel adequately trained to integrate the management of this diagnosis or prevention efforts into everyday practice. Furthermore, the respondents were not active in routine anticipatory guidance with adolescents for prevention of alcohol-affected pregnancies. The development, dissemination, and implementation of best practice tools for prevention, diagnosis, and referral of fetal alcohol syndrome that are specific for general and subspecialist pediatricians are recommended.

Female↗
PubMed2004

[Adult fetal alcohol syndrome (FAS) with various nouropsychiatric symptoms].

This is the first report of an adult patients with the fetal alcohol syndrome (FAS) in Japan, who was treated for psychiatric disorders. The case was a 35 years-old woman who had many neuropsychiatric symptoms. She had been treated for 15 years at the Kurihama Alcoholism Center, for mental retardation, schizophrenic symptoms, attention deficit hyperactivity disorder, learning disorder, trichotillomania, bipolar disorder, and impulsive behavior. She had low body weight at birth, mental retardation and a small facial malformation, which were diagnosed as FAS. At first admission, she was not diagnosed as FAS because her parent denied that her mother drank during pregnancy. Recently, her family admitted her mother's heavy drinking during pregnancy, and we diagnosed her as having FAS. She showed many pathological symptoms of the central nervous system such as very lower scores for performance IQ than for verbal IQ in the WAIS-R and enlargement of the lateral ventricle on MRI. Recently many reports have mentioned that prenatal alcohol exposure brings about severe damage of the central nervous system. Therefore, one author proposes that such disorders are referred to as fetal alcohol spectrum disorders (FASD). This patient showed many symptoms of FASD, and was difficult to treat because of these symptoms.

Adult↗
PubMed2006

Prenatal alcohol exposure (PAE) reduces the size of the forepaw representation in forepaw barrel subfield (FBS) cortex in neonatal rats: relationship between periphery and central representation.

Prenatal alcohol exposure (PAE) alters limb development that may lead to structural and functional abnormalities of the limb reported in children diagnosed with Fetal Alcohol Spectrum Disorder. To determine whether PAE alters the central representation of the forelimb we used the rodent barrel cortex as our model system where it was possible to visualize and quantitatively measure the size of the forepaw representation in the forepaw barrel subfield (FBS) in first somatosensory cortex. In the present study, we examined the effects of PAE on pattern and size of the forepaw and forepaw representation in FBS in neonatal rats at gestational day 32 that corresponds to postnatal day 9. Pregnant Sprague-Dawley rats were chronically intubated with binge doses of ethanol (6 g/kg) from gestational day 1 through gestational day 20. The offspring of the ethanol treated dams comprised the ethanol (EtOH) group. The effect of PAE on the EtOH group was compared with a nutritional-controlled pairfed (PF) group and a normal chowfed (CF) group. The ventral (glabrous) surface area of the forepaw digits, length of digit 2 through digit 5, and the corresponding glabrous forepaw digit representations in the FBS were measured and compared between treatment groups. In rats exposed to in utero alcohol, the sizes of the overall glabrous forepaw and forepaw digits were significantly reduced in EtOH pups compared to CF and PF pups; overall glabrous forepaw area was 11% smaller than CF controls. Glabrous digit lengths were also smaller in EtOH rats compared to CF controls and significantly smaller in digit 2 through digit 4. The glabrous digit representation in FBS was 18% smaller in the EtOH group when compared to the CF treatment. However, PAE did not produce malformations in the forepaw or alter the pattern of the forepaw representation in FBS; instead, PAE significantly reduced both body and brain weights compared to controls. Unexpectedly, little or no correlation was observed between the size of the glabrous forepaw compared to the size of the glabrous forepaw representation in the FBS for any of the treatment groups. The present findings of PAE-related alterations in sensory periphery and the central cortical representation may underlie deficits in sensorimotor integration reported among children with Fetal Alcohol Spectrum Disorder.

Alcohol-Induced Disorders, Nervous System↗
PubMed2003

A mouse model of prenatal ethanol exposure using a voluntary drinking paradigm.

BACKGROUND: The incidence of fetal alcohol spectrum disorders is estimated to be as high as 1 in 100 births. Efforts to better understand the basis of prenatal ethanol-induced impairments in brain functioning, and the mechanisms by which ethanol produces these defects, will rely on the use of animal models of fetal alcohol exposure (FAE). METHODS: Using a saccharin-sweetened alcohol solution, we developed a free-choice, moderate alcohol access model of prenatal alcohol exposure. Stable drinking of a saccharin solution (0.066%) was established in female mice. Ethanol then was added to the saccharin in increasing concentrations (2%, 5%, 10% w/v) every 2 days. Water was always available, and mice consumed standard pellet chow. Control mice drank saccharin solution without ethanol. After a stable baseline of ethanol consumption (14 g/kg/day) was obtained, females were impregnated. Ethanol consumption continued throughout pregnancy and then was decreased to 0% in a step-wise fashion over a period of 6 days after pups were delivered. Characterization of the model included measurements of maternal drinking patterns, blood alcohol levels, food consumption, litter size, pup weight, pup retrieval times for the dams, and effects of FAE on performance in fear-conditioned learning and novelty exploration. RESULTS: Maternal food consumption, maternal care, and litter size and number were all found to be similar for the alcohol-exposed and saccharin control animals. FAE did not alter locomotor activity in an open field but did increase the time spent inspecting a novel object introduced into the open field. FAE mice displayed reduced contextual fear when trained using a delay fear conditioning procedure. CONCLUSIONS: The mouse model should be a useful tool in testing hypotheses about the neural mechanisms underlying the learning deficits present in fetal alcohol spectrum disorders. Moreover, a mouse prenatal ethanol model should increase the opportunity to use the power of genetically defined and genetically altered mouse populations.

Alcohol Drinking↗
PubMed2004

Fetal alcohol syndrome prevention in Washington State: evidence of success.

Fetal alcohol syndrome (FAS) is a permanent birth defect syndrome caused by maternal consumption of alcohol during pregnancy. It is characterised by growth deficiency, central nervous system damage/dysfunction, and a unique cluster of minor facial anomalies. To assess the effectiveness of fetal alcohol syndrome prevention efforts, one must be able to estimate accurately the prevalence of fetal alcohol syndrome over time in population-based samples. With the establishment of the Washington State Fetal Alcohol Syndrome Diagnostic and Prevention Network of clinics, the development of the Fetal Alcohol Syndrome Facial Photographic Analysis Software, the creation of the Fetal Alcohol Spectrum Disorders (FASD) 4-Digit Diagnostic Code, the establishment of the Foster Care Fetal Alcohol Syndrome Screening Program, and the collection of Pregnancy Risk Assessment Management System data on maternal use of alcohol during pregnancy, the tools, methods and infrastructure for assessing the effectiveness of fetal alcohol syndrome primary prevention efforts in Washington State are in place. A cross-sectional study was conducted to determine whether the prevalence of fetal alcohol syndrome among children in a foster care population, born between 1993 and 1998, decreased with the documented decrease in prevalence of maternal use of alcohol during pregnancy from 1993 and 1998 in Washington State. The prevalence of maternal drinking during pregnancy in Washington State declined significantly (P < 0.001) from 1993 to 1998 as did the prevalence of fetal alcohol syndrome among foster children born 1993-98 (P < 0.03). These observations support the likelihood that fetal alcohol syndrome prevention efforts in Washington State are working successfully.

Alcohol Drinking↗
PubMed2025

Discovery of a DNA methylation episignature as a molecular biomarker for fetal alcohol syndrome.

PURPOSE: Fetal alcohol spectrum disorder (FASD) encompasses a range of clinical features and neurodevelopmental disorders in children exposed to alcohol in utero. Despite its global public health significance, FASD diagnosis remains challenging because of nonspecific clinical findings and the lack of an accurate molecular diagnostic biomarker. This study aimed to evaluate peripheral blood DNA methylation (DNAm) profiles as a potential diagnostic biomarker for fetal alcohol syndrome. METHODS: Genomic DNAm profiles from 93 individuals with suspected or confirmed FAS, including a clinically diagnosed FAS subgroup, were analyzed and compared with a large database of control and patient cohorts with previously reported DNAm episignatures. Functional analysis of these DNAm profiles was performed to identify episignatures and assess their potential diagnostic utility. RESULTS: A relatively sensitive and specific DNAm episignature for FAS was identified. Comparative epigenomic analysis revealed functional correlations between FAS and other rare genetic disorders, supporting the robustness of the identified DNAm profiles as a diagnostic tool. CONCLUSION: This study demonstrates that unique DNAm profiles provide a robust episignature biomarker for FAS. These findings contribute to the molecular understanding of FAS and hold promise for improving diagnostic accuracy for this complex disorder.

Humans↗
PubMed2006

Association of attention deficit hyperactivity disorder and gestational alcohol exposure: an exploratory study.

OBJECTIVE AND METHODS: To explore association between prevalence of ADHD and levels of risk for gestational alcohol exposure, the authors reviewed the charts of 2,231 youth referred for fetal alcohol spectrum disorders. Participants were categorized into four groups by different levels of risk for gestational alcohol exposure. For each group, the prevalence rates of ADHD and other selected disorders were determined. RESULTS: The disorder ranking first in overall prevalence was ADHD (41%), followed by learning disorder (17%) and oppositional-defiant/conduct disorder (16%). Prevalence rates of ADHD across the groups generally were high risk > some risk > unknown risk > no risk. CONCLUSION: The frequency distribution of ADHD cases was according to the levels of risk for gestational alcohol exposure. These results add to a growing body of evidence supporting an association between ADHD and prenatal alcohol exposure. Findings need to be confirmed by definitive studies on ADHD and gestational alcohol exposure.

Alcoholism↗
PubMed2005

Alcohol consumption in pregnant, black women is associated with decreased plasma and erythrocyte docosahexaenoic acid.

BACKGROUND: Inner-city, black women are among those groups that are at higher risk for having infants with fetal alcohol spectrum disorders that can include life-long neurobehavioral and cognitive impairments. Chronic alcohol consumption can decrease amounts of docosahexaenoic acid (DHA), a fatty acid that is essential for optimal infant neural and retinal development in a variety of tissues. METHODS: Black women who presented at an inner-city antenatal clinic for their first prenatal visit were recruited into a longitudinal, observational study. Alcohol intake was determined by a structured interview. Participants provided blood specimens and completed food frequency surveys at 24 weeks of gestation, infant delivery, and 3 months postpartum. Fatty acid composition analyses were completed on 307, 260, and 243 for plasma and 278, 261, and 242 erythrocyte specimens at 24 weeks of gestation, delivery, and 3 months postpartum, respectively. RESULTS: Proportion of drinking days at the first prenatal visit was associated with decreased DHA in plasma and erythrocytes throughout the study. This association was the strongest at 24 weeks of gestation. In addition, an interaction between proportion of drinking days at the time of conception and ounces of absolute alcohol per drinking day at the time of conception was detected and demonstrated that, in daily drinkers, high intakes of alcohol are associated with decreased DHA and arachidonic acid (AA) concentrations in plasma. CONCLUSIONS: Frequent and high intakes of alcohol that have been previously associated with fetal alcohol spectrum disorders are also associated with decreased maternal DHA and AA plasma concentrations. The present findings indicate that maternal DHA deficiency is associated with high-risk drinking and may contribute to the mechanism(s) of alcohol-related neurodevelopmental disorders.

Adult↗
PubMed2005

"Do I know what I need to do?" A social communication intervention for children with complex clinical profiles.

PURPOSE: Speech-language pathologists frequently address social communication difficulties in children with diverse clinical profiles. The purpose of this study was to investigate the feasibility of a social communication intervention for a school-age child with a complex cognitive and behavioral profile secondary to diagnosis of a fetal alcohol spectrum disorder. METHOD: A case study is presented to describe the implementation of the intervention targeting mental state verb production and social cognitive skills. The intervention included group role play of social scripts and a checklist to elicit the participant's statements about others' perspectives and strategies for completing the social script. Treatment data monitored the participant's responses to the checklist questions. Probe sessions, consisting of theory of mind false belief tasks, were used to examine mental state verb use. RESULTS: Treatment data demonstrated that the participant stated more strategies in response to checklist questions. The participant did not produce any mental state verbs during baseline probes, but did produce mental state verbs during the treatment phase. CLINICAL IMPLICATIONS: The results support use of this intervention to change children's linguistic and social cognitive skills. Suggestions for extending this intervention to include a generalization plan targeting classroom social communication interactions are provided.

Behavior↗
PubMed1994

Alcohol, marijuana, and tobacco: effects of prenatal exposure on offspring growth and morphology at age six.

Little is known about the long-term effects of prenatal exposure to alcohol. There are even fewer reports on the longitudinal effects of exposure to either marijuana or tobacco during pregnancy. This study is on the 6-year follow-up of 668 children enrolled in the Maternal Health Practices and Child Development Project. Mothers were interviewed at the 4th and 7th months of pregnancy, and mothers and children were evaluated at delivery, 8, and 18 months, and 3 and 6 years postpartum. At 6 years of age, children who were exposed to alcohol prenatally were significantly smaller in weight, height, head circumference, and palpebral fissure width. These effects on size were mediated by the effect of prenatal alcohol exposure on the offspring at 8 months. Prenatal alcohol exposure was also significantly associated with maternal reports of the child's appetite at 6 years. There were no effects of prenatal marijuana or tobacco exposure on growth when the children were age 6. There were also no significant relationships between prenatal exposure to alcohol, marijuana, or tobacco and the rate of morphologic anomalies, including the features of the fetal alcohol syndrome.

Alcohol Drinking↗
PubMed2006

Comparison of motor delays in young children with fetal alcohol syndrome to those with prenatal alcohol exposure and with no prenatal alcohol exposure.

BACKGROUND: Researchers are increasingly considering the importance of motor functioning of children with fetal alcohol spectrum disorder (FASD). The purpose of this study was to assess the motor development of young children with fetal alcohol syndrome (FAS) to determine the presence and degree of delay in their motor skills and to compare their motor development with that of matched children without FAS. METHODS: The motor development of 14 children ages 20 to 68 months identified with FAS was assessed using the Vineland Adaptive Behavior Scales (VABS). In addition, 2 comparison groups were utilized. Eleven of the children with FAS were matched for chronological age, gender, ethnicity, and communication age to: (1) 11 children with prenatal alcohol exposure who did not have FAS and (2) 11 matched children without any reported prenatal alcohol exposure. The motor scores on the VABS were compared among the 3 groups. RESULTS: Most of the young children with FAS in this study showed clinically important delays in their motor development as measured on the VABS Motor Domain, and their fine motor skills were significantly more delayed than their gross motor skills. In the group comparisons, the young children with FAS had significantly lower Motor Domain standard (MotorSS) scores than the children not exposed to alcohol prenatally. They also had significantly lower Fine Motor Developmental Quotients than the children in both the other groups. No significant group differences were found in gross motor scores. For MotorSS scores and Fine Motor Developmental Quotients, the means and standard errors indicated a continuum in the scores from FAS to prenatal alcohol exposure to nonexposure. CONCLUSIONS: These findings strongly suggest that all young children with FAS should receive complete developmental evaluations that include assessment of their motor functioning, to identify problem areas and provide access to developmental intervention programs that target deficit areas such as fine motor skills. Fine motor delays in children with FAS may be related to specific neurobehavioral deficits that affect fine motor skills. The findings support the concept of an FASD continuum in some areas of motor development.

Adaptation, Psychological↗
PubMedDate not supplied

Fetal alcohol syndrome: neuropsychiatric phenomics.

Fetal alcohol syndrome (FAS) is a common developmental disorder with impairments in multiple neuropsychiatric spheres of varying severity. Few population-derived studies of the behavioral phenotype are available. The purpose of this study was to estimate the prevalence of neuropsychiatric disorders in three groups: subjects who met criteria for FAS (n=152); subjects who met criteria for partial FAS/ARND (n=150); and referred subjects who did not meet criteria for either FAS or partial FAS/ARND (n=86). Each subject had a standardized evaluation by a medical geneticist. All subjects were from North Dakota. We found increases in the prevalence rates of neuropsychiatric disorders in subjects with FAS compared to subjects with partial FAS/ARND and the lowest rates in the group that did not meet criteria for either FAS or partial FAS/ARND. Comorbid attention deficit hyperactivity disorder occurred in 73% of cases with FAS, in 72% cases with partial FAS/ARND, and in 36% subjects who did not meet criteria for either. For other neuropsychiatric disorders, a similar distribution of comorbidity was found. This study supports the concept of a continuum of impairment resulting from prenatal alcohol exposure. The presence of complex cognitive, behavioral, and physical symptomatology in the affected subjects with prenatal alcohol exposure would seem to fit well under the diagnostic rubric of fetal alcohol spectrum disorder (FASD). Diagnosis and long-term management will require increasing access to multidisciplinary child development teams including mental health professionals who treat children and adolescents. Adults will require care primarily from teams with expertise in mental health and developmental disabilities.

Adolescent↗
PubMed2006

Games that "work": using computer games to teach alcohol-affected children about fire and street safety.

Unintentional injuries are a leading cause of death and disability for children. Those with developmental disabilities, including children affected by prenatal alcohol exposure, are at highest risk for injuries. Although teaching safety skills is recommended to prevent injury, cognitive limitations and behavioral problems characteristic of children with fetal alcohol spectrum disorder make teaching these skills challenging for parents and teachers. In the current study, 32 children, ages 4-10, diagnosed with fetal alcohol syndrome (FAS) and partial FAS, learned fire and street safety through computer games that employed "virtual worlds" to teach recommended safety skills. Children were pretested on verbal knowledge of four safety elements for both fire and street safety conditions and then randomly assigned to one condition. After playing the game until mastery, children were retested verbally and asked to "generalize" their newly acquired skills in a behavioral context. They were retested after 1 week follow-up. Children showed significantly better knowledge of the game to which they were exposed, immediately and at follow-up, and the majority (72%) was able to generalize all four steps within a behavioral setting. Results suggested that this is a highly effective method for teaching safety skills to high-risk children who have learning difficulties.

Child↗
PubMed2005

Fetal alcohol syndrome: an assessment of the field.

Fetal exposure to alcohol is the major known cause of mental retardation in the Western world. For more than half of the 20th century, the placenta was widely believed to be an effective barrier against environmental agents. The discovery that offspring of pregnant women who were exposed to German measles or administered thalidomide were often malformed raised awareness that teratogens could be any environmental agent, including viruses and drugs, that caused abnormal development. Alcohol was not identified as a teratogen until the 1970s. Fetal exposure to alcohol can cause fetal alcohol syndrome (FAS), which is characterized by specific physical traits and central nervous system dysfunctions. The development of animal model systems has facilitated our study of the effects of fetal alcohol exposure and the elucidation of the mechanisms involved in alcohol-induced abnormal development. Despite our current understanding of the effects of fetal alcohol exposure, the occurrence of FAS and associated fetal alcohol spectrum disorders is still widespread and the associated health-care costs are staggering. This symposium provides an up-to-date analysis of fetal exposure to alcohol and FAS. It is directed not only to investigators working in the field but to a diverse group of scientists working in the biological and biomedical fields to stimulate cross-disciplinary awareness, interest, and collaboration.

Alcohol Drinking↗