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Choline is essential for healthy cognitive development. Single nucleotide polymorphisms (SNPs; rs3199966(G), rs2771040(G)) within the choline transporter SLC44A1increase risk for choline deficiency. In a choline intervention trial of children who experienced prenatal alcohol exposure (PAE), these alleles are associated with improved cognition.

Fetal alcohol spectrum disorders (FASD) are developmental disabilities that are estimated to occur in 2–5% of elementary school children and that negatively impact a child's ability to function without support. Timely diagnosis‐informed interventions are crucial to optimizing the developmental trajectory of children with FASD. The true prevalence of FASD among children receiving services for developmental disabilities is unknown. An FASD prevalence study was carried out between 2011 and 2014 among a sample of 5‐ to 7‐year‐old children who were receiving services provided by the California State Regional Center for Developmental Disabilities in San Diego County. Children whose parent or caregiver consented were evaluated using the Collaboration on Fetal Alcohol Spectrum Disorders Prevalence study assessment protocol and classification criteria. Among 216 eligible caregiver‐child dyads, 44 completed assessments that were sufficient to obtain a classification for FASD, including fetal alcohol syndrome (FAS), partial FAS, alcohol‐related neurodevelopmental disorder, or no fetal alcohol spectrum disorder. Fifteen children were classified as meeting the criteria for an FASD. A minimum FASD prevalence rate of 69.4 per 1000 (6.9%) among all eligible children was estimated. None of the children classified as FASD were receiving services because of an FASD diagnosis, and none had previously been diagnosed with FASD. Autism was the most common qualifying diagnosis for which children classified as FASD were receiving services. The 6.9% prevalence estimate among Regional Center clients was higher than the prevalence estimate of 2.3% in the same community among 5‐ to 7‐year‐old children in the general population, though the estimate was based on only 20% of eligible dyads. All children in the sample were receiving Regional Center services for another diagnosis. Barriers to eligibility for services for children with FASD may lead to less than optimum care for these children. Study findings support the facilitation of access to developmental services for children with FASD. An FASD prevalence study was carried out among a sample of 5‐7‐year old children receiving services provided by the California State Regional Center for Developmental Disabilities in San Diego County. Among 216 eligible children, 44 completed assessments, and fifteen met criteria for an FASD. A minimum FASD prevalence rate of 69.4 per 1,000 (6.9%) was estimated. None of the children identified had previously been diagnosed with FASD. Study findings support facilitation of access to developmental services for children with FASD.

Although the effects of prenatal alcohol exposure (PAE) have been studied extensively, there is relatively little information available on adult mental health functioning among exposed individuals. The current study compares the self‐reported midlife mental health status of individuals who were prenatally exposed to alcohol and diagnosed in childhood with the effects of this exposure with that of unexposed individuals. Participants (N= 292) were recruited from two longitudinal cohorts in Atlanta and Seattle and asked to complete an Adult Health Questionnaire that surveyed their current health and mental health status. The questionnaire was completed either in‐person or remotely and included questions about current symptoms of depression and anxiety and mental health disorder diagnoses. The analysis compared a Nonexposed Contrast group to those in two exposure groups: (1) Alcohol Exposed with Fetal Alcohol Effect but not meeting criteria for Fetal Alcohol Syndrome (FAS) and (2) Alcohol Affected and meeting criteria for FAS. Both alcohol‐exposed groups reported higher levels of current depressive symptoms and a higher prevalence of diagnoses of depression, anxiety, bipolar disorder, and/or attention deficit/hyperactivity disorder. No differences were noted for psychotic disorders. PAE was also associated with greater environmental stressors, including higher levels of adverse childhood events and lower current socioeconomic status. Path analyses suggested that PAE was indirectly related to mood disorders with its effects being mediated by other environmental factors. PAE is associated with greater rates of mental health disorders in middle adulthood. These outcomes appear to result from multiple stressors that affect individuals made vulnerable by their early alcohol exposure. Clinical outcomes could be improved by prevention efforts directed at preventing prenatal alcohol use and reducing environmental stressors later in life, and by the early identification of PAE and its effects. A long‐term follow up of adults from two longitudinal cohorts with prenatal alcohol exposure (PAE) finds an association with significantly increased rates of mental health disorders at midlife as well as adverse early life events. Outcomes appear to result from multiple stressors affecting individuals made vulnerable by their early exposure. Clinical outcomes could be improved by prevention efforts directed at both prenatal alcohol use and later environmental stressors, and by early identification of PAE and its effects.

This study aimed to develop an efficient and easily calculable risk score that can be used to identify an individual's risk of having been exposed to alcohol prenatally. Data for this study were collected as part of the Collaborative Initiative on Fetal Alcohol Spectrum Disorders, Phases 2 and 3. Two cohorts (ages 5 to 17 years) completed a comprehensive neurobehavioral battery and a standard dysmorphology exam: a development cohort (DC; n= 325) and a comparative cohort (CC; n= 523). Both cohorts included two groups: those with histories of heavy prenatal alcohol exposure (AE‐DC, n= 121; AE‐CC, n= 177) and a control group that included subjects with minimal or no prenatal alcohol exposure (CON‐DC, n= 204; CON‐CC, n= 346). Behavioral assessments and physical exam data were combined using regression techniques to derive a risk score indicating the likelihood of prenatal alcohol exposure. Subjects were then divided into two subgroups: (1) low risk and (2) high risk. Chi‐square (χ2) determined classification accuracy and ROC curves were produced to assess the predictive accuracy. Correlations between risk scores and intelligence quotient and executive function scores were calculated. Subjects were accurately classified in the DC (χ2= 78.61, p< 0.001) and CC (χ2= 86.63, p< 0.001). The classification model also performed well in the DC (ROC = 0.835 [SE = 0.024, p< 0.001]) and CC (ROC = 0.786 [SE = 0.021, p< 0.001]). In the AE‐CC and CON‐CC, there were modest but significant associations between the risk score and executive function (AE‐CC: r= −0.20, p= 0.034; CON‐CC: r= −0.28, p< 0.001) and intelligence quotient (AE‐CC: r= −0.20, p= 0.034; CON‐CC: r= −0.28, p< 0.001). The risk score significantly distinguished alcohol‐exposed from control subjects and correlated with important cognitive outcomes. It has significant clinical potential and could be easily deployed in clinical settings. A risk score was created using physical exam and behavioral assessment variables that indicates the likelihood of prenatal alcohol exposure. The score accurately identified alcohol‐exposed from control subjects with and without clinical concerns, and was moderately but significantly related to intellectual and executive functioning. The risk score could be simply deployed in a clinical setting and has significant clinical potential as an early screening tool.

Cognitive and behavioral sequelae of prenatal alcohol exposure (PAE) continue to be prevalent in the United States and worldwide. Because these sequelae are also common in other neurodevelopmental disorders, researchers have attempted to identify a distinct neurobehavioral profile to facilitate the differential diagnosis of fetal alcohol spectrum disorders (FASD). We used an innovative, individual participant meta‐analytic technique to combine data from six large U.S. longitudinal cohorts to provide a more comprehensive and reliable characterization of the neurobehavioral deficits seen in FASD than can be obtained from smaller samples. Meta‐analyses were performed on data from 2236 participants to examine effects of PAE (measured as oz absolute alcohol/day (AA/day)) on IQ, four domains of cognition function (learning and memory, executive function, reading achievement, and math achievement), sustained attention, and behavior problems, after adjusting for potential confounders using propensity scores. The effect sizes for IQ and the four domains of cognitive function were strikingly similar to one another and did not differ at school age, adolescence, or young adulthood. Effect sizes were smaller in the more middle‐class Seattle cohort and larger in the three cohorts that obtained more detailed and comprehensive assessments of AA/day. PAE effect sizes were somewhat weaker for parent‐ and teacher‐reported behavior problems and not significant for sustained attention. In a meta‐analysis of five aspects of executive function, the strongest effect was on set‐shifting. The similarity in the effect sizes for the four domains of cognitive function suggests that PAE affects an underlying component or components of cognition involving learning and memory and executive function that are reflected in IQ and academic achievement scores. The weaker effects in the more middle‐class cohort may reflect a more cognitively stimulating environment, a different maternal drinking pattern (lower alcohol dose/occasion), and/or better maternal prenatal nutrition. These findings identify two domains of cognition—learning/memory and set‐shifting—that are particularly affected by PAE, and one, sustained attention, which is apparently spared. We used an innovative, individual participant meta‐analytic technique to combine data from six large U.S. longitudinal cohorts to provide a more comprehensive and reliable characterization of the neurobehavioral deficits seen in FASD than can be obtained from smaller samples. Prenatal alcohol exposure (PAE) effects on cognitive function were stronger than for behaviour problems or sustained attention. This analysis identified two domains of cognition—learning/memory and set‐shifting—that are particularly affected by PAE, and one domain, sustained attention, which is spared.

Few studies have investigated the partner's influence on risk factors such as alcohol consumption and depression during pregnancy. Partner substance use and lower relationship satisfaction predict higher maternal alcohol use and depressive symptoms. Because prenatal alcohol use and maternal depression affect infant outcomes, it is imperative to examine how the partner affects these maternal risk factors. The current study examined the effect of a latent construct of partner influence on maternal alcohol use and depressive symptoms, and the effects on infant development of these maternal factors. Participants were 246 pregnant women from 2 sites in Western Ukraine from whom longitudinal data were collected as part of a multisite study. In the first trimester, mothers reported on relationship satisfaction, partner substance use, and socioeconomic status (SES). In the third trimester, they reported on alcohol use and depressive symptoms. Infants were assessed using the Bayley Scale of Infant Development (average age = 6.93 months). A latent construct titled partner influence was formed using partner substance use and measures of relationship satisfaction, including the frequency of quarreling, happiness in the relationship, and the ease of talking with the partner. Using structural equation modeling, a model was specified in which partner influence and SES predicted maternal alcohol use and depressive symptoms, which in turn predicted infant neurodevelopmental outcomes. Higher partner influence significantly predicted lower prenatal alcohol use and lower depressive symptoms, controlling for the effect of SES. Higher maternal prenatal alcohol use significantly predicted lower infant mental and psychomotor development. Maternal depressive symptoms did not predict infant development over and above the effect of alcohol use. Partner influence is an important contributor to prenatal alcohol use and maternal depressive symptoms, over and above the effect of SES. The significant paths from prenatal alcohol exposure to infant neurodevelopmental outcomes underscore the importance of partner influence during pregnancy. We used structural equation modeling to understand the influence of the partner on maternal prenatal alcohol use and depressive symptoms, and the effect of these prenatal risk factors on the infant at six months. Partner influence was a latent construct made up of three relationship variables and two partner substance use variables. Controlling for socioeconomic status, partner influence significantly predicted alcohol use and depressive symptoms during the third trimester. Further, higher alcohol use predicted lower infant development at six months.

Evidence suggests that prenatal alcohol exposure (PAE) may adversely impact insulin production and signaling but there is limited information on the range of these effects and their future health consequences. A prospective cohort of predominantly African‐American individuals identified while in utero and followed into adulthood were used to evaluate differences in various indicators of diabetes, including fasting plasma glucose, hemoglobin A1c (HbA1c), and insulin levels. The homeostatic model assessment of insulin resistance (HOMA‐IR) was also computed. Body mass index (BMI) was calculated and normal defined as < 25 kg/m2. Participants were categorized as having PAE (n= 39) if their mothers drank at least 1 ounce of absolute alcohol per week or more during the 1sttrimester of pregnancy and as Controls (n= 22) if their mothers reported abstaining from alcohol consumption during pregnancy. Mean age of the sample was 36.0 ± 1.5 years. Indices of glucose metabolism, including fasting plasma glucose and hemoglobin A1c levels, did not vary by group status but insulin levels and HOMA‐IR values varied by group status and BMI level. PAE individuals with a normal BMI had lower insulin levels than Controls. However, in PAE subjects, there was a steeper increase in insulin levels relative to their BMI than in Control subjects. A cluster of 5 PAE cases had low levels of insulin and 4 of the 5 had severe cognitive impairment. The bidirectional effects on insulin level and insulin resistance associated with PAE may indicate differential rates of diabetes disease impact or differential PAE impact in the brain and peripheral areas involved in insulin production and signaling. These alterations may contribute to the metabolic disease risk associated with PAE. The metabolic health consequences of prenatal alcohol exposure (PAE) were evaluated in a prospective cohort of African American individuals (36.0 ± 1.5 years). Although no differences were found in glucose metabolism, insulin levels and homoeostatic model assessment of insulin resistance (HOMA‐IR) differed. PAE individuals with a normal BMI had lower insulin compared to Controls but had steeper increases in insulin levels relative to their BMI. These alterations may contribute to their metabolic disease risk and have implications for preventative healthcare.

Rating scales are designed to complement traditional performance‐based measures, and both can provide useful information about the functioning of youth with histories of prenatal alcohol exposure. Few studies, however, have compared ratings from multiple informants or the relationship between these subjective rating scale scores and the objective results from laboratory performance‐based scales. The current study addressed both of these questions in 3 study groups: children with histories of prenatal alcohol exposure (n= 47), attention‐deficit/hyperactivity disorder (ADHD; n= 41), and typically developing controls (CON; n= 73). All subjects completed a standardized neuropsychological test battery, including laboratory measures of executive functioning and a self‐report measure of executive function behaviors. Parents and teachers completed corresponding rating scales of executive function behaviors for each subject. This study assessed the relationship between these behavior rating scales and corresponding neuropsychological tests, and interrater agreement among the multiple informants. Weak correlations were found between the rating scales and laboratory measures, indicating poor convergent validity for the behavior rating scale. Interrater reliability was found but it differed by group. Agreement was found between parent and teacher ratings for children with prenatal alcohol exposure, whereas teacher–child agreement was found for those with ADHD. Findings from this study indicate that behavior ratings can be used to supplement laboratory measures but may not be measuring cognitive abilities regardless of whether a clinical diagnosis is present. A multimethod approach should be used when measuring skills in this domain. This was one of the first studies to examine cross‐informant agreement in a sample of children with prenatal alcohol exposure. Further research is necessary to understand why interrater agreement differed for children with prenatal alcohol exposure and those with ADHD. This study assessed the relationship between behavior ratings of executive function and neuropsychological measures in children with prenatal alcohol exposure (AE), attention‐deficit/hyperactivity disorder (ADHD), and typically developing controls (CON). Weak correlations were found between the two types of measures. Parent‐teacher agreement was significant for the AE group, not significant for the ADHD group, and mixed for the CON group. Findings reveal that parents and teachers of alcohol‐exposed children report similar difficulties but emphasize the importance of using a multi‐method approach when determining deficits in this domain.

Prenatal alcohol exposure (PAE) has been identified as one of the leading preventable causes of developmental disabilities, but early identification of those impacted has been challenging. This study evaluated the use of infant cardiac orienting responses (CORs), which assess neurophysiological encoding of environmental events and are sensitive to the impact of PAE, to predict later fetal alcohol spectrum disorder (FASD) status. Mother–infant dyads from Ukraine were recruited during pregnancy based on the mother’s use of alcohol. Participants (n= 120) were then seen at 6 and 12 months when CORs were collected and in the preschool period when they were categorized as having (i) fetal alcohol syndrome (FAS), (ii) partial FAS (pFAS), (iii) alcohol‐related neurodevelopmental disorder (ARND), (iv) PAE and no diagnosis, or (v) no PAE and no diagnosis. To assess CORs, stimuli (auditory tones and pictures) were presented using a fixed‐trial habituation/dishabituation paradigm. Heart rate (HR) responses were aggregated across the first 3 habituation and dishabituation trials and converted to z‐scores relative to the sample’s mean response at each second by stimuli. Z‐scores greater than 1 were then counted by condition (habituation or dishabituation) to compute a total risk index. Significant group differences were found on total deviation scores of the CORs elicited from visual but not auditory stimuli. Those categorized as pFAS/FAS had significantly higher total deviation scores than did those categorized as ARND or as having no alcohol‐related diagnosis with or without a history of PAE. Receiver operating characteristic curve analysis of the visual response yielded an area under the curve value of 0.765 for predicting to pFAS/FAS status. A score reflecting total deviation from typical HR during CORs elicited using visual stimuli in infancy may be useful in identifying individuals who need early intervention as a result of their PAE.

In children with prenatal alcohol exposure, spatial working memory is affected and brain regions important for spatial working memory performance exhibit atypical neurodevelopment. We therefore hypothesized that children with prenatal alcohol exposure may also have atypical development of spatial working memory ability. We examined the relation between spatial working memory and age using a cross‐sectional developmental trajectory approach in youth with and without histories of heavy prenatal alcohol exposure. The Cambridge Neuropsychological Test Automated Battery Spatial Working Memory subtest was administered to children 5.0 to 16.9 years old. While the controls and children with prenatal alcohol exposure showed similar performance at younger ages, larger group differences were observed in older children. This effect was replicated in a separate sample. The atypical brain development that has previously been reported in children with heavy prenatal alcohol exposure may have clinically relevant implications for cognitive development; however, longitudinal cognitive analyses are needed. While young children with heavy prenatal alcohol exposure make equivalent amounts of errors and utilize a similar strategy as controls on the CANTAB Spatial Working Memory Test, by age 16 there is nearly a whole standard deviation difference between the groups on these two performance measures. This cross‐sectional data suggests that children with prenatal alcohol exposure develop the cognitive abilities necessary for spatial working memory at a slower rate than controls.

The effects of prenatal alcohol exposure (PAE) are conceptualized as fetal alcohol spectrum disorder, with fetal alcohol syndrome (FAS) as the most severe. Many find it more difficult to characterize behavioral and cognitive effects of exposure on the central nervous system when physical signs are not present. In the current study, an operational definition of alcohol‐related neurodevelopmental disorder (ARND) was examined to determine its usefulness in discrimination of children classified as ARND based on behavior (ARND/B) and cognition (ARND/C) from children in 4 contrast groups: (i) children exposed to study‐defined “risky drinking”; (ii) children with any reported PAE; (iii) children classified as “Higher Risk” for developmental problems; and (iv) children classified as “Lower Risk.” A total of 1,842 children seen as part of a surveillance study (J Am Med Assoc, 319, 2018, 474) were evaluated for alcohol exposure and physical characteristics of FAS, and completed neurodevelopmental testing. Ninety‐one were identified as either ARND/B or ARND/C and contrasted with other groups to further identify distinguishing patterns. Multinomial logistic regression (MLR) was used to examine the accuracy of classification and to identify factors contributing to such classification. Children described as ARND/C were distinct from other groups based on cognition and behavior as well as demographic factors (e.g., age, race, SES), child characteristics (e.g., gestational age; sex), and other drug exposures, while those described as ARND/B differed only on behavior and other drug exposures. MLR models successfully discriminated ARND groups from children in other groups with accuracy ranging from 79% (Higher Risk) to 86.7% (Low Risk). ARND has been a subject of debate. This analysis suggests the effects of alcohol on behavior and cognition even in the absence of the characteristic facial features and growth deficiency that can be identified. The results also indicate that it may be possible to distinguish such children from those in other high‐risk groups. Alcohol Related Neurodevelopmental Disorder was operationalized and evaluated as part of the Fetal Alcohol Spectrum Disorders. Criteria for classification based on behavior (ARND/B) and cognition (ARND/C) was applied to first grade children and compared to groups exposed to study‐defined “risky drinking”, those classified as developmentally “Higher Risk”, and as “Low Risk” and found that ARND can be distinguished by behavior, cognition, and certain demographic factors. Results demonstrate that prenatal alcohol exposure affects behavior in the absence of physical features.

AbstractObjective:Polyunsaturated fatty acids are vital for optimal fetal neuronal development. The relationship between maternal alcohol consumption and smoking with third trimester plasma fatty acids were examined and their association with Fetal Alcohol Spectrum Disorders (FASD).Methods:Moderate to heavy alcohol-using and low/unexposed comparison women were recruited during mid-pregnancy from two prenatal clinics in Ukraine. The participants’ infants underwent physical and neurobehavioral exams prior to one-year of age and classified as having FASD by maternal alcohol consumption and neurobehavioral scores. A subset of mother-child pairs was selected representing three groups of cases and controls: Alcohol-Exposed with FASD (AE-FASD, n = 30), Alcohol-Exposed Normally Developing (AE-ND, n = 33), or Controls (n = 46). Third trimester maternal plasma samples were analyzed for fatty acids and levels were compared across groups.Results:The percent of C18:0 (p < 0.001), arachidonic acid (AA, C20:4n-6, p = 0.017) and C22:5n-6 (p = 0.001) were significantly higher in AE-FASD women than controls or AE-ND women. Alcohol-exposed women who smoked had lower C22:5n-3 (p = 0.029) and docosahexaenoic acid (DHA, C22:6n-3, p = 0.005) and higher C22:5n-6 (p = 0.013) than women consuming alcohol alone or abstainers.Conclusion:Alterations in fatty acid profiles were observed in moderate to heavy alcohol-consuming mothers with infants classified with FASD compared to alcohol-exposed normally developing infants or controls.

This study examined the relationship between prenatal exposure to alcohol, manifested through fetal alcohol syndrome (FAS) and pFAS, and hypertension in children and adolescents. This study was designed to analyze the association between fetal alcohol spectrum disorders (FASD) Status and hypertension status. FAS/pFAS‐diagnosed respondents (n= 125) were collected from a FASD Clinical database in Atlanta, Georgia. Non‐FAS/pFAS respondents (n= 500) were taken from the National Health and Nutrition Examination Survey (NHANES). Chi‐square analyses were used to examine the extent to which FASD status, sex, race/ethnicity, medication use, and obesity status each related to hypertension status. A logistic regression was performed analyzing the relationship between FASD status (y/n: independent) and hypertension status (y/n: dependent) while controlling for age, sex, race/ethnicity, medication use, and obesity status. Univariate relationships between hypertension status and FASD status (OR = 8.46, p< 0.001), medication use (OR = 3.25, p< 0.001), and obesity status (OR = 3.03, p= 0.02) proved to be statistically significant (p< 0.05). FASD status significantly predicted hypertension status (β= 2.31, OR = 10.06, p< 0.001) after accounting for age, sex, race/ethnicity, medication use, and obesity status. The major findings of this study suggest a significant relationship between FASD and hypertension in youth. Race/ethnicity and obesity also proved important in predicting hypertensive blood pressure readings independent of FASD diagnosis. Further research is needed to isolate prenatal alcohol exposure (PAE) as a factor promoting increased hypertension and to assess the risk for hypertension in alcohol‐affected adults. The relationship between FASDand hypertension in clinically‐referred children and adolescents was investigated. Logistic regression indicated a significant predictive relationship between FASDand elevations in both systolic and diastolic blood pressure after controlling for age, sex, race/ethnicity, medication use, and obesity status. Race/ethnicity and obesity also proved significant in predicting hypertension independently of FASDdiagnosis. Further research is needed to isolate prenatal alcohol exposure as a factor in youth hypertension and to assess the risk for hypertension in alcohol‐affected adults.

Youth with heavy prenatal alcohol exposure have high rates of behavioral concerns and psychopathology, including increased oppositional and conduct behaviors. The relation between those concerns and executive function (EF) deficits is unknown. We investigated the association of oppositional and conduct behavior and EFin adolescents to inform targeted intervention. Subjects (N = 267) ages 10 to 17 years comprised 3 groups: alcohol‐exposed with oppositional/conduct behaviors (AE+), alcohol‐exposed without oppositional/conduct behaviors (AE−), and controls (CON). Group differences on direct neuropsychological (Delis‐Kaplan Executive Function System [D‐KEFS]) and indirect parent‐report (Behavior Rating Inventory of Executive Function [BRIEF]) EFmeasures were tested with multivariate analysis of covariances, followed by univariate analysis of variances and pairwise comparisons. The contribution of attention‐deficit/hyperactivity disorder (ADHD) within the AEgroups was assessed in secondary analyses. On the D‐KEFS, there was an omnibus main effect of group, with significant main effects on 3 of 6 variables (CON>AE+, AE−). Within the AEgroups, ADHDdid not alter the results. On the BRIEF, there was an omnibus significant main effect of group, with significant main effects on all scales (CON

Considered the leading cause of developmental disabilities worldwide, fetal alcohol spectrum disorders (FASD) are a global health problem. To take advantage of neural plasticity, early identification of affected infants is critical. The cardiac orienting response (COR) has been shown to be sensitive to the effects of prenatal alcohol exposure and is an inexpensive, easy to administer assessment tool. The purpose of this study was to evaluate the COReffectiveness in assessing individual risk of developmental delay. As part of an ongoing longitudinal cohort study in Ukraine, live‐born infants of women with some to heavy amounts of alcohol consumption in pregnancy were recruited and compared to infants of women who consumed low or no alcohol. At 6 and 12 months, infants were evaluated with the Bayley Scales of Infant Development‐II. CORs were also collected during a habituation/dishabituation learning paradigm. Using a supervised logistic regression classifier, we compared the predictive utility of the CORindices to that of the 6‐month Bayley scores for identification of developmental delay based on 12‐month Bayley scores. Heart rate collected at each second (Standard COR) was compared to key features (Key COR) extracted from the response. Negative predictive values (NPV) were 85% for Standard COR, 82% for Key COR, and 77% for the Bayley, and positive predictive values (PPV) were 66% for Standard COR, 62% for Key COR, and 43% for the Bayley. Predictive analysis based on the CORresulted in better NPVand PPVthan the 6‐month Bayley score. As the resources required to obtain a Bayley score are substantially more than in a COR‐based paradigm, the findings are suggestive of its utility as an early scalable screening tool based on the COR. Further work is needed to test its long‐term predictive accuracy. Early identification of neurodevelopmentally impaired infants is critical. Infants of women with varying amounts of alcohol consumption in pregnancy were given a cardiac orienting response (COR) paradigm at 6 months and the Bayley Scales of Infant Development‐II at both 6 and 12 months. The COR robustly outperformed a 6‐month Bayley score in predicting 12‐month delay. This is suggestive of the CORs utility as an early, scalable screening tool as substantially more resources are required to generate a Bayley score.

Prenatal alcohol exposure (PAE) has been found to impact neurophysiological encoding of environmental events negatively in the first year of life but has not been evaluated in older infants or toddlers. Cardiac orienting responses (ORs) collected during a habituation/dishabituation learning paradigm were obtained from 12‐ to 18‐month‐olds to assess the impact of PAEbeyond the first year of life. Participants included women and their toddlers who differed in PAEhistories and enrolled in a randomized clinical trial of multivitamin/mineral usage during pregnancy. Those who were randomly assigned to the no intervention group were used for this analysis. The habituation/dishabituation paradigm consisted of 10 habituation and 5 dishabituation trials. Baseline heart rate (HR) was collected for 30 seconds prior to stimulus onset, and responses to the stimuli were assessed by sampling HRfor 12 seconds poststimulus onset. The speed of the ORin response to auditory stimuli in the dishabituation condition was found to be altered as a function of maternal alcohol use around conception. For visual stimuli, positive histories of PAEwere predictive of the magnitude but not the speed of the response on habituation and dishabituation trials. A history of binge drinking was associated with reduced magnitude of the ORresponse on visual encoding trials, and level of alcohol exposure at the time of conception was predictive of the magnitude of the response on visual dishabituation trials. Cardiac ORs collected in the toddler period were sensitive to the effects of PAE. The magnitude of the ORwas more sensitive to the impact of PAEthan in previous research with younger infants, and this may be a function of brain maturation. Additional research assessing the predictive utility of using ORs in making decisions about individual risk was recommended. Prenatal alcohol exposure (PAE) has been found to impact neurophysiological encoding of environmental events in the first year of life but has not been evaluated beyond the first year of life. Toddler's cardiac orienting responses (OR) collected during a habituation/dishabituation learning paradigm were sensitive to the effects of PAE. The magnitude of the ORwas more sensitive to the impact of PAEthan in previous research with younger infants, and this may be a function of brain maturation.

Neurobehavioral consequences of heavy prenatal alcohol exposure are well documented; however, the role of age or sex in these effects has not been studied. The current study examined the effects of prenatal alcohol exposure, sex, and age on neurobehavioral functioning in children. Subjects were 407 youth with prenatal alcohol exposure (n =192) and controls (n =215). Two age groups (child [5 to 7 years] or adolescent [10 to 16 years]) and both sexes were included. All subjects completed standardized neuropsychological testing, and caregivers completed parent‐report measures of psychopathology and adaptive behavior. Neuropsychological functioning, psychopathology, and adaptive behavior were analyzed with separate 2 (exposure history) × 2 (sex) × 2 (age) multivariate analyses of variance (MANOVAs). Significant effects were followed by univariate analyses. No 3‐way or 2‐way interactions were significant. The main effect of group was significant in all 3 MANOVAs, with the control group performing better than the alcohol‐exposed group on all measures. The main effect of age was significant for neuropsychological performance and adaptive functioning across exposure groups with younger children performing better than older children on 3 measures (language, communication, socialization). Older children performed better than younger children on a different language measure. The main effect of sex was significant for neuropsychological performance and psychopathology; across exposure groups, males had stronger language and visual spatial scores and fewer somatic complaints than females. Prenatal alcohol exposure resulted in impaired neuropsychological and behavioral functioning. Although adolescents with prenatal alcohol exposure may perform more poorly than younger exposed children, the same was true for nonexposed children. Thus, these cross‐sectional data indicate that the developmental trajectory for neuropsychological and behavioral performance is not altered by prenatal alcohol exposure, but rather, deficits are consistent across the 2 age groups tested. Similarly, observed sex differences on specific measures were consistent across the groups and do not support sexually dimorphic effects in these domains.

Prenatal alcohol exposure (PAE) is an established risk factor for neurodevelopmental deficits in the offspring. Prenatal depression has been associated with neurodevelopmental deficits in the offspring, although investigations into unmedicated prenatal depression have been inconsistent. We hypothesized that unmedicated prenatal depressive symptoms would independently and jointly with PAE predict neurodevelopmental outcomes in infant offspring. We studied 344 participants from a randomized clinical trial of multivitamin supplements in pregnant women in Ukraine. Women were recruited based upon periconceptional alcohol use and followed up to 12 months postpartum. Prenatal depressive symptoms were assessed at approximately 32 weeks of gestation using the Beck Depression Inventory score. Neurodevelopment was assessed with the Bayley Scales of Infant Development II Mental Development Index (MDI) and Psychomotor Development Index (PDI) at 6 and 12 months postpartum. Generalized linear regression models were constructed to assess the independent and joint effects of prenatal depressive symptoms and PAE in models adjusted for sociodemographic and pregnancy characteristics. PAE was independently associated with deficits in neurodevelopmental outcomes at 6 and 12 months, however, level of prenatal depressive symptoms was not. We found marginal evidence of synergism of depressive symptoms and PAE, with larger deficits in those with both exposures observed for the PDI‐6 months (p= 0.05) and MDI‐12 months (p= 0.09). Additionally, there was a suggestion of sexual dimorphism; females had stronger deficits from joint exposures than males (depressive symptom [MDI‐6 months] female: −8.28, 95% CI −13.06, −3.49; male: 0.68, 95% CI −4.58, 5.94; pfor interaction 0.04). While not statistically significant for the MDI or PDI at 12 months, the trend persisted. Infants exposed to PAE and prenatal depression may be at an increased risk of neurodevelopmental deficits. Healthcare providers should be aware of this possible synergism in their efforts to mitigate the neurodevelopmental effects of these co‐occurring exposures. From a sample of pregnant women in Ukraine recruited based upon periconceptional alcohol use, we found prenatal alcohol exposure (PAE) was independently associated with deficits in neurodevelopmental outcomes at 6 and 12 months; however, level of prenatal depressive symptoms was not. We found marginal evidence of synergism of PAEand depressive symptoms in neurodevelopmental assessments. Healthcare providers should be aware of this possible synergism in their efforts to mitigate the neurodevelopmental effects of these co‐occurring exposures.

Despite the prevalence of fetal alcohol spectrum disorders (FASD) and the importance of accurate identification of patients, clinical diagnosis may not be consistent across sites due to the heterogeneous nature of FASDand the characteristics of different diagnostic systems used. Here, we compare 5 systems designed to operationalize criteria recommended for the diagnosis of effects of prenatal alcohol exposure (PAE). We determined the extent of consistency among them as well as factors that may reduce intersystem reliability. Compared are: Emory Clinic, Seattle 4‐Digit System (Diagnostic Guidelines for Fetal Alcohol Spectrum Disorders: The 4‐Digit Diagnostic Code, Seattle, WA, University Publication Services, 2004), Centers for Disease Control and Prevention (Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis, Department of Health and Human Services, Centers for Disease Control and Prevention, Atlanta, GA, 2004), Canadian Guidelines (CMAJ, 172, 2005, S1), and the Hoyme Modifications (Pediatrics, 115, 2005, 39). Subjects were 1,581 consecutively registered patients applying for evaluation at a university‐based clinic treating alcohol and drug‐exposed children. Records of the multidisciplinary evaluation (pediatric, social, psychological) were abstracted. Diagnostic criteria for all 5 systems were applied, and patients were diagnosed according to each of the systems. We compared results using Cohen's Kappa to evaluate the extent of agreement. Percent of individuals diagnosed with FASDranged from 4.74% (CDC) to 59.58% (Hoyme). Examination using Cohen's Kappa found modest agreement among systems, particularly when individual diagnoses, Fetal Alcohol Syndrome (FAS), partial FAS(pFAS), and Alcohol‐Related Neurodevelopmental Disorder (ARND) were used. Examination of diagnostic criteria found almost perfect agreement on growth (weight; height), with limited overlap for physical features (palpebral fissures, hypoplastic philtrum, upper vermillion) and for neurobehavioral outcomes. Child's race and age influenced agreement among systems, with African American and older children more frequently diagnosed. Results suggest problems in convergent validity among these systems, as demonstrated by a lack of reliability in diagnosis. Absence of an external standard makes it impossible to determine whether any system is more accurate, but outcomes do suggest areas for future research that may refine diagnosis. Five systems were compared to evaluate the convergent validity of the diagnosis of fetal alcohol spectrum disorders (FASD). The figure shows a map in which each case (N= 1581) is represented as a single line color coded for diagnostic category, showing limited consensus among commonly used systems in diagnosis of children with prenatal alcohol exposure. Both age of child and ethnicity also affected outcomes. The results suggest the need for a consensus approach in revision of the diagnostic criteria for FASD.

Fetal alcohol spectrum disorders (FASD) are often characterized by disruptive behavior problems and there are few effective interventions available. GoFARis a novel, 3‐part intervention designed to improve self‐regulation and adaptive living skills of children with FASDby improving metacognitive control of emotions and arousal. The intervention has 3 components: (i) GoFAR: a “serious game” designed to teach a metacognitive control strategy in a computer game environment; (ii) parent training on child behavioral regulation; and (iii) Behavior Analog Therapy (BAT) sessions, a practical application of the metacognitive learning methodology by parent and child in the context of learning adaptive skills. The learning strategy (FAR) teaches the child to Focus and make a plan, Act out the plan, and Reflect back on the plan. Thirty families were randomized to 3 groups: (i) GoFAR(n= 10); (ii) FACELAND(n= 10); or (iii) CONTROL (n= 10). The 2 intervention groups, GoFARand FACELAND, used computer games to instruct children. Both groups also received 5 sessions of parent training followed by 5 sessions of joint parent/child therapy (BAT). Assessment of disruptive behavior, including frequency of temper tantrums, frustration tolerance, impulsivity, destructiveness, aggression, and maintaining attention were carried out before enrollment at Mid‐Treatment, when game play and parent training were completed, and finally, after completing the BATsessions. Parental report of disruptive behavior overall was significantly reduced in the GoFARgroup after the first components, game play and parent training, and after the BATsessions in the FACELANDgroup with no changes in the CONTROLgroup over time. The GoFAR®game was well received by children and effective in teaching the required skills. Mastering the FARmetacognitive strategy was associated with a reduction in disruptive behaviors in children with FASDsuggesting that effective interventions can improve outcomes for this high‐risk group.

(Abstracted from JAMA2018;319(5):474–482)Several single-site, active-case ascertainment studies in the United States have shown widely varying prevalence estimates for fetal alcohol spectrum disorders, composed of fetal alcohol syndrome, partial fetal alcohol syndrome, and alcohol-related neurodevelopmental disorder. Prevalence of fetal alcohol spectrum disorders are challenging to estimate using routine surveillance methods, and cases are often misdiagnosed or undiagnosed.

Background: Neurocognitive effects of prenatal alcohol exposure in adulthood are not well documented. Questions persist regarding the extent to which there are specific, measurable effects beyond those associated with global ability deficits, whether individuals without the full fetal alcohol syndrome (FAS) demonstrate alcohol‐related cognitive impairments, and whether observed memory effects are specific to a particular modality, i.e., verbal vs. visual/spatial domains.

Background: Increased systemic oxidant stress contributes to a variety of maternal complications of pregnancy. Although the antioxidant glutathione (GSH) and its oxidized component glutathione disulfide (GSSG) have been demonstrated to be significantly altered in the adult alcoholic, the effects of maternal alcohol use during pregnancy on oxidant stress in the postpartum female remain under investigation. We hypothesized that maternal alcohol use would increase systemic oxidant stress in the pregnant female, evidenced by an oxidized systemic GSH redox potential.

Background: While behavioral studies have established that prenatal alcohol exposure (PAE) can result in diminished arithmetic processing capability, the underlying neural correlates of this deficit are still unclear. The aim of the present study was to use functional magnetic resonance imaging to determine the effect of PAE on neuronal activation during a subtraction task.

Background: Fetal alcohol syndrome (FAS) has been recognized as a disabling condition with a significant impact on the neurobehavioral functioning of affected individuals, including cognition, behavior, and academic functioning, but little research has been performed on targeted interventions for these children.

Abstract: Background: Using methodologies from developmental studies on infant information‐processing skills, early manifestations of later long‐term neurocognitive effects of prenatal alcohol exposure can be explored by assessing primary cognitive processes, including attentional regulation and processing speed.

This article represents the proceedings of a symposium at the 2002 Research Society on Alcoholism/International Society for Biomedical Research on Alcoholism meeting in San Francisco, CA. The organizers were Edward P. Riley and Sarah N. Mattson, and the chairperson was Edward P. Riley. The presentations were (1) Neurobehavioral deficits in alcohol‐exposed South African infants: preliminary findings, by Sandra W. Jacobson, Christopher D. Molteno, Denis Viljoen, and Joseph L. Jacobson; (2) A pilot study of classroom intervention for learners with fetal alcohol syndrome in South Africa, by Colleen Adnams, M. W. Rossouw, M. D. Perold, P. W. Kodituwakku, and W. Kalberg; (3) Differential effects of prenatal alcohol exposure on fluid versus crystallized intelligence, by P. W. Kodituwakku, W. Kalberg, L. Robinson, and P. A. May; (4) Neurobehavioral outcomes of prenatal alcohol exposure: early identification of alcohol effects, by Claire D. Coles; (5) Fetal alcohol syndrome in Moscow, Russia: neuropsychology test performance, by Sarah N. Mattson, E. P. Riley, A. Matveeva, and G. Marintcheva; and (6) Long‐term follow‐up of Finnish children exposed to alcohol in utero in various durations, by Marit I. Korkman and I. Autti‐Rämö. The discussant was Ting‐Kai Li.

Background: Sustained attention problems and impulsivity are reported in association with prenatal alcohol exposure and fetal alcohol syndrome, but research in this area is limited and contradictory.

Behavioral deficits are often noted in children with fetal alcohol syndrome (FAS) and other individuals with prenatal alcohol exposure, including mental retardation, learning problems, social problems, and deficits in attention. Because attention deficit, hyperactivity disorder (ADHD) has been diagnosed so frequently in children with FAS and other alcohol related birth defects, there has been speculation that alcohol is an etiological factor in ADHD. To examine the relationship between behavior characteristics of children with fetal alcohol exposure and those seen in children with a diagnosis of ADHD, 149 low socioeconomic status (SES), African‐American children (mean age = 7.63 years) were given a battery of neuropsychological and behavioral tests. One hundred and twenty‐two were a sub‐sample from a longitudinal study of prenatal alcohol exposure, whereas twenty‐seven were identified in an ADHD Clinic. Children were given two sets of tests: (1) “traditional model” of conventional behavioral and psychiatric measures of ADHD and externalizing behavior; and (2) measures of neurocognitive functioning reflecting a four‐factor model of the neurological basis of the components of attention (Mirsky AF, in Integrated Theory and Practice in Clinical Neuropsychology, Hillsdale, NJ, Lawrence Erlbaum Associates, 1989). Results indicated that children with the physical characteristics associated with prenatal alcohol exposure and those with a diagnosis of ADHD had equivalent intellectual abilities with both clinical groups performing more poorly than contrast children from the same SES and ethnic groups. However, there were clear distinctions on behavioral and neurocognitive measures between the two clinical groups with those with ADHD performing more poorly on conventional tests sensitive to attentional problems and conduct disorder. When these two groups were compared on measures designed to measure the model of the four factors of attention by Mirsky, they were noted to have distinct patterns of deficits. These results suggested that the alcohol‐affected children did not have the same neurocognitive and behavioral characteristics as children with a primary diagnosis of ADHD.

In two experiments, 24 college women and 48 housewives and businesswomen in Atlanta, Georgia, volunteered to fill out questionnaires to investigate sexual, personality, and demographic variables associated with the reading of best-selling erotic romances. While there were some differences in the results obtained from younger and older women, readers tended to be between 25 and 35 years old (mean age = 30.6) while nonreaders were either younger or older. No differences between readers and nonreaders were found in marital status, income, or education. Measures of traditional versus liberal attitudes toward women's roles, locus of control, self-esteem, and intimacy were similar for both groups. Readers and nonreaders of erotic romances reported different motives for recreational reading (escape versus self-knowledge) and read different kinds of books. Readers reported having sexual relations twice as ofter per week as nonreaders and stated that they frequently used fantasy as a complement to intercourse, while nonreaders did so rarely or never. It was concluded that erotic romances provide a form of sexual stimulation for their readers similar to that provided by sexual fantasies and that they are a form of “soft-core” pornography that women find socially acceptable and nonthreatening.