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. Author manuscript; available in PMC: 2025 Feb 1.
Published in final edited form as: Alcohol Clin Exp Res (Hoboken). 2024 Jan 8;48(2):400–408. doi: 10.1111/acer.15256

Parenting with fetal alcohol spectrum disorders and neurobehavioral outcomes in offspring

Gaby J Ritfeld 1,2,3,4, Michael Wang 4, Zvi Shapiro 3, Julie A Kable 3, Claire D Coles 3
PMCID: PMC10922647  NIHMSID: NIHMS1954834  PMID: 38149361

Abstract

Background:

The neurobehavioral health impairments associated with prenatal alcohol exposure (PAE) are now known to persist through adulthood. However, little is known about how these impairments affect parenting abilities and neurobehavioral health of offspring. This study compares parents with fetal alcohol spectrum disorder (FASD) with non-exposed parents and assessed the neurobehavioral health of their children.

Methods:

49 parent-child dyads were recruited from a longitudinal cohort with a low socioeconomic status. Measures included the Parenting Styles and Dimensions Questionnaire, Family Support Scale, an in-depth psychosocial history, the Pediatric Symptom Checklist (PSC; parent and child reports), the Achenbach Child Behavior Checklist (CBCL), a screening psychiatric evaluation of the child, the NIH Toolbox Cognition Battery for Children, The Vineland Adaptive Behavior Scales-Third Edition caregiver rating form, and the Traumatic Events Screening Inventory (parent and child reports).

Results:

Cognitive functioning was impaired for both offspring of parents with FASD (x̄=81.1, SD 13.0) and control parents (x̄=79.9, SD 16.1), but despite similar impairments, children of parents with FASD were less likely to have an Individualized Education Plan than controls. Adaptive functioning was adequate for both groups (x̄ =92.1, SD 15.4 in exposed vs x̄ =94.3, SD 12.3 in controls) and CBCL and PSC scores in both groups were within normal limits. Parents in both groups showed a predominantly authoritative parenting style. Despite similar adverse childhood event frequency in both groups, parents with FASD were less likely to recognize their child’s adverse experiences.

Conclusion:

Parents with FASD display notable strengths including a predominantly authoritative parenting style. However, parents with FASD underrecognize child trauma and show an underutilization of developmental services compared to socioeconomically matched controls, despite similar neurocognitive impairments. Impairments in adaptive functioning in parents with FASD may translate into difficulties with child-parent communication, insight into neurobehavioral problems, and advocacy skills. There is a need to identify and support parents with FASD to optimize their parenting abilities in the context of their individual strengths and difficulties.

Keywords: Fetal alcohol spectrum disorders, prenatal alcohol exposure, intergenerational effects, adverse childhood experiences

INTRODUCTION

Fetal alcohol spectrum disorders (FASD) affect approximately 5% of the population (May et al., 2018, 2014) and is the leading cause of congenital brain damage in the United States. The teratogenic effects of prenatal alcohol exposure (PAE) are well established in children and young adults and include psychiatric disorders, neurocognitive deficits, and impairments in adaptive and social functioning (Coles et al., 2010; May et al., 2014; O’Connor and Paley, 2009). Studies also show high rates of exposures to adverse childhood experiences (ACEs) in families affected by substance use which further contribute to poor outcomes in children and young adults with FASD (Mukherjee et al., 2018; Reuben et al., 2016). In contrast, the effects of PAE in mature adults have only recently become the focus of systematic investigation. Specifically, Coles and her colleagues investigated the mental and social health outcome of a cohort of midlife adults, who were identified at birth as prenatally exposed to alcohol, and periodically assessed in childhood, adolescence, and young adulthood. Data from this investigation show that adults affected by PAE have persistent impairments in adaptive, social, and cognitive functioning, and poorer mental health than unexposed controls (Coles et al., 2022, 2010; Shapiro et al., 2023). Many adults in this sample now have children of their own but little is known about the impact of FASD on the ability to parent and/or on the characteristics of children whose parents are alcohol-affected.

Data suggest high prevalence of substance use disorders in individuals with FASD (Bingol et al., 1987; Streissguth et al., 1996, 2004), which puts their offspring at increased risk for prenatal alcohol exposure and FASD. In addition, several animal studies have been conducted that point towards multigenerational transmission of prenatal alcohol effects, unrelated to in utero alcohol exposure of the second-generation fetus. Specifically, offspring of mice prenatally exposed to alcohol have been shown to have lower birth weight (Becker and Randall, 1987) and offspring of rats prenatally exposed to alcohol have been shown to have slower neonatal growth as well as neurobehavioral impairments (Lam et al., 2000). Although the mechanisms of multigenerational transmission of these effects are unclear, several hypotheses can be conceptualized. It has become increasingly evident in the past two decades that prenatal exposures significantly affect adult health and disease through a process referred to as fetal programming (Barker, 1997). Since the introduction of this concept by Barker et al., a growing literature has established relationships between prenatal nutritional deficiencies affecting metabolic and vascular systems and impacting disease development later in life, e.g. diabetes, hypertension, stroke and cancer (Barker et al., 2006, 2006, 2002; Barker, 2006, 2002). The mechanisms of these effects are only starting to be elucidated and may include alterations at the epigenetic, cellular, organ-structural, and hormonal-axes levels. It can thus be hypothesized that the effects of fetal programming in adults with FASD (F1 generation) also impacts their reproductive systems and their offspring’s prenatal and postnatal health (F2 generation). Alternatively, transmission of alcohol effects to the F2 generation can be hypothesized to occur through direct (epi)genetic effects of alcohol on the alcohol exposed F1 generation gametes, while the F1 generation parent was him/herself still in utero. Thirdly, transmission of prenatal alcohol effects could occur without direct alcohol exposure by germline transmission of alcohol-induced genetic or epigenetic alterations (Mead and Sarkar, 2014). Although human studies investigating this are lacking, recent evidence for epigenetic transgenerational transmission of prenatal alcohol effects has been proposed in a rodent study, showing hypermethylation of the proopiomelanocortin (POMC) gene (which gives rise to several pituitary peptide hormones, including the HPA-axis regulatory hormone ACTH), induced by fetal alcohol exposure, which was transmitted to the F2 and F3 generation through male, but not female germline (Govorko et al., 2012). This and other epigenetic research is starting to elucidate mechanisms through which transmission of prenatal alcohol affects may occur (Chastain and Sarkar, 2017; Mead and Sarkar, 2014).

Parenting with FASD may pose unique challenges that affect offspring as well. Rutman and Van Bibber have conducted a qualitative study on the challenges that parents with FASD face by conducting semi-structured interviews on a sample of individuals with (suspected) FASD, which highlighted the experienced challenges and barriers associated with the effects of FASD and the need for ongoing support for adults with FASD (Rutman and Van Bibber, 2010). Rutman and Van Bibber conceptualized areas where FASD-related disabilities may pose specific challenges to parenting. For example, alcohol effects like impairments in working memory, executive functioning and judgment may make it more difficult to negotiate the environment effectively to keep oneself and one’s child safe, while also ensuring adequate child development. Mental health disorders may impact the parent-child relationship. Likewise, substance use disorders may make involvement with child and family protective services more likely (Lander, Howsare and Byrne, 2013). Furthermore, stigma and limited understanding of disabilities associated with FASD may compromise effective formation of alliances with support systems and resources. Indeed, Rutman and Van Bibber (2010) found that parents with (suspected) FASD report low likelihood of seeking help for their disabilities out of fear as being labeled as “unfit” parents. The importance and effectiveness of support systems and intervention programs focused on decreasing risk of mothers affected by substance use to offspring, is highlighted by the work of Grant and colleagues (Grant et al., 2005; Rasmussen et al., 2012), which, through the development of the Parent-Child Assistance Program focuses on the prevention of FASD in the next generation. More recently, young women with FASD have also become the subjects of these health-promoting interventions, with outcomes including decreased substance use and more stable housing (Grant et al., 2004). However, second-generation offspring have not been studied, and without accurate knowledge about effects of prenatal alcohol exposure on parenting and offspring, it will be hard for policy makers and health care workers to respond in effective ways. Figure 1 summarizes possible mechanisms of multigenerational transmission of prenatal alcohol effects.

Figure 1:

Figure 1:

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Possible mechanisms of multigenerational transmission of prenatal alcohol effects. Created with BioRender.com.

In addition to consideration of the FASD-specific parental factors and parenting styles affecting outcomes, there are many other conceivable risk and resilience factors affecting outcome, including race, ethnicity, and socioeconomic status (Abel and Hannigan, 1995). Adverse childhood experiences (ACEs) in particular are known to have a profound impact on health and functioning (Bellis et al., 2014; Felitti et al., 1998), may be more common and likely to contribute to poor outcomes in individuals with FASD (Mukherjee et al., 2018), and can be transmitted to future generations (Negriff et al., 2020).

The effects of parental disabilities on parent-child-interactions, socio-economic functioning, and risk for adversity, combined with possible (epi)genetic transmission of prenatal alcohol effects, place offspring of individuals with FASD in a vulnerable position. For individuals with FASD, it is known that early recognition and intervention of prenatal alcohol effects mitigates risk of poor outcomes (Streissguth et al., 2004), and the same may be true for their offspring. It is therefore imperative we have knowledge about the second-generation health outcomes of FASD as well as risk and resilience factors moderating outcome, so that if multigenerational transmission of prenatal alcohol effects indeed exists, policymakers, caregivers and health care workers can make decisions and provide support, resources and treatment to help affected individuals and decrease risk for future generations.

The aims of our investigation were 1) To assess the neurobehavioral health status of the offspring of adults with FASD, including frequency of psychiatric problems, aspects of neurocognitive and adaptive functioning, and 2) To identify parenting challenges of individuals with FASD that may pose risks of transgenerational transmission of adversity related to PAE, as well as parenting strengths that may foster transgenerational resilience. We hypothesize that 1) offspring of adults with FASD have poorer neurobehavioral outcomes than offspring of unexposed controls, 2) parenting ability is affected in parents with FASD, and 3) parents with FASD utilize fewer developmental and mental health resources for their children compared to control parents.

METHODS

Recruitment and data collection

Parents for this study were recruited from a group of mostly African American, disadvantaged individuals whose mothers were recruited while they were in utero to participate in a prospective longitudinal study on the impact of heavy prenatal alcohol exposure, a cohort which contains both individuals with prenatal alcohol exposure and nonexposed controls. Participants who had previously participated in this longitudinal study and had endorsed having children between the ages of 5 and 17 were recruited by phone or e-mail. If they had multiple eligible children, they were asked to enroll their eldest child within this age range. Data collection took place both through teleconference and in-person at the investigator’s clinical site. Consent and assent were obtained from caregivers and children, respectively. Approval for this study was obtained from the Emory University’s Institutional Review Board.

Measures

An initial caregiver interview was conducted to collect information on family demographics, income, (history of) living arrangements, custody situation(s), prenatal alcohol use, birth complications, birth height, birth weight, child medical problems, child and family mental problems, academic functioning, and services received. Whether a family was living below the poverty line was calculated using a Federal Poverty Level calculator. To assess for behavioral and emotional problems and competencies, caregivers were asked to fill out an Achenbach Child Behavior Checklist (Achenbach, 2017). The CBCL/1½−5 was used for children 5 years of age and the CBCL/6–18 was used for children 6 years and older. Both CBCL’s yield Total Problems Scores, Internalizing and Externalizing Problems Scores, and Total Competency Scores, and these scales have a standardized mean T score of 50, with a standard deviation of 10. Higher scores represent more problems on the Total Problems Scale, and Internalizing and Externalizing Problems Scale. The Total Competency Scale includes items to assess for participation in extracurricular activities, social competence and school performance, with lower scores representing lower functioning in these areas. In addition, children underwent a psychiatric interview and mental status examination, and both parents and children completed the pediatric symptom checklist. The pediatric symptom checklist is 35-item recognition tool for psychosocial dysfunction, rated on a 3-point Likert scale. For the parent report, a score of 28 or higher indicates psychological impairment. For the child report, this cutoff score is 30 (Jellinek et al., 1999).

To obtain a standard measure of cognitive functioning in the children, the NIH Toolbox Cognition Battery was used (Akshoomoff et al., 2014). For children ages 7–17, this battery includes: 1. Flanker Inhibitory Control and Attention Test, a 3-minute measure of executive function that assesses attention and inhibition of automatic responses; 2. Dimensional change card sort Test, a 4-minute measure of executive functioning that assesses cognitive flexibility; 3. List Sorting Working Memory, a 7-minute measure of working memory that assesses immediate recall and sequencing of stimuli. 4. Picture Sequence Memory Test, a 7-minute measure of episodic memory that assesses cognitive processes involved in acquisition, storage, and retrieval of new information; 5. Pattern Comparison Processing Speed Test, a 3-minute test that assesses the amount of information that can be processed within a certain unit of time; 6. Picture Vocabulary Test, a 4-minute test assessing receptive vocabulary; 7. Oral reading recognition Test, a 3-minute test measuring reading decoding skills. These tests yield the summarizing Cognitive Function Composite Score. For children aged 5–6, the NIH Toolbox Cognition Battery includes the Flanker Inhibitory Control and Attention Test, Picture Sequence Memory Test, Picture Vocabulary Test and Dimensional Change Card Sort Test, and yields the summarizing Early Childhood Composite Score. The standardized mean for these measures is 100, with a standard deviation of 15. Parent Full-Scale IQ was measured at a prior time point of this longitudinal cohort study, when these individuals were young adults, using the Wechsler Adult Intelligence Scale. The standardized mean for this measure is 100, with a standard deviation of 15.

The Vineland Adaptive Behavior Scales-Third Edition caregivers rating form was administered to caregivers to assess adaptive functioning in the children (Sparrow et al., 1984). This measure yields both an overall adaptive behavior composite score and three domain scores for communication, socialization, and daily living skills. The standardized mean score for this measure is 100, with a standard deviation of 15.

The Parenting Styles and Dimensions Questionnaire (PSDQ) and Family Support Scale were obtained from caregivers to characterize parenting style and degree of family support, respectively. The PSDQ is a 32-item, parent-report questionnaire, rated on a 5-point Likert Scale which yields subscores on three types of parenting styles: authoritative (high responsiveness and high demandingness), indulgent (high responsiveness and low demandingness), and authoritarian (low responsiveness and high demandingness), with higher scores reflecting that the parent demonstrates more of that specific parenting style (Monaghan et al., 2012). The Family Support Scale is an 18-item survey that assesses how helpful 20 sources of support are for the parents in caring for their child, and is rated on a 5-point Likert scale with higher scores reflecting greater perceived support, and total scores ranging from 0 to 100.

To assess for adverse childhood experiences, the 16-item Traumatic Events Screening Inventory (TESI-C) was administered to the children/adolescents and the 7-item Traumatic Events Screening Inventory (TESI-PRR) was administered to parents. The reported traumatic events were summed to form a total TESI-C or TESI-PRR score, respectively. The TESI discrepancy score was then calculated by subtracting the sum of the TESI-C by the sum of the TESI-PRR. The discrepancy score thus indicates the difference in the number of traumatic events reported by the child and the number of traumatic events reported by the parent.

Parent reports of school performance were categorized into excellent, average, and poor performance. The excellent category includes reports of “straight A’s”, “honor student”, and “A’s and B’s”. Average performance includes “mostly B’s”, “average”, and “B’s and C’s.” Poor performance includes “D’s”, “C’s”, “low average”, and “failing”.

Data analysis

Descriptive statistics and frequency distributions were used as the first level of analysis. Two-tailed T-tests were used to assess for differences in numerical outcomes between children of exposed parents and controls. Chi-squared testing was used to determine differences in categorical outcomes between these two groups. Statistical significance was accepted at p < 0.05.

RESULTS

Demographic data

Results are included for 49 parent-child dyads. 28 are offspring of parents with FASD and 21 are offspring of parents without FASD. Table 1 summarizes the demographic data for the cohorts. A large proportion of our participants lived below the federal poverty line, in single-parent households and most participants were African American. Data for 46 births showed that 12 (24.5%) were preterm (<37 weeks of pregnancy). Most parents were unable to report their child’s height and weight at birth.

TABLE 1.

DEMOGRAPHIC DATA

Total sample Control Cohort FASD Cohort p - value
Sex
 Male 48% 52% 44% p = .59
Race
 African American 92% 91% 93% p = .72
 Mixed 8% 9% 7% p = .72
Mean child age (standard deviation) 12.2 12.9 (2.9) 11.6 (3.4) p = .16
Household information
 Single parent 65% 76% 55% p = .28
Under poverty line a 37% 38% 37% p = .94
Premature birth 25% 38% 15% p = .065
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a

The federal poverty level as defined by the Department of Health and Human Services, which takes into account annualized income and number of household members

Parent characteristics

Table 2 summarizes the parent characteristics data. Parents with FASD showed a statistical trend towards more alcohol use during pregnancy compared to mothers without FASD (29% vs 9.5 %, respectively; p=.089). There were no differences between groups in parenting style, family support scale scores, or parental IQ scores. Parental IQ scores were below average in both groups.

TABLE 2.

OUTCOME DATA

Total Control Cohort FASD Cohort p - value
Maternal alcohol use during pregnancy
 More than once a month 22.4% 9.5% 29% p = .09
Mean CBCLa (standard deviation)
 Total score 51.2 50.3 (11.6) 52.0 (12.4) p = .64
 Competency score 42.4 42.9 (12.1) 42.0 (11.5) p = .81
Mean Vinelandb (standard deviation) 93.8 95.7 (14.6) 92.4 (15.2) p = .46
Mean Cognitionc (standard deviation)
 Child 80.6 79.9 (16.1) 81.1 (13.0) p = .82
 Parent 82.4 84.0 (13.1) 81.4 (14.2) p = .53
Reported academic performance
 Excellent 49% 62% 41% p = .39
 Average 38% 24% 48% p = .39
 Poor 12% 14% 11% p = .39
Mean PSCd (standard deviation)
 Parent reported 14.3 11.8 (8.3) 16.0 (10.1) p = .18
 Youth reported 25.0 25.1 (9.3) 25.0 (8.7) p = .98
Mean PSDe (standard deviation)
 Authoritative 4.0 4.1 (.6) 4.0 (.5) p = .58
 Authoritarian 2.1 2.1 (.6) 2.2 (.5) p = .55
 Permissive 2.1 2.0 (.3) 2.1 (.4) p = .57
Medical condition present in child
 Yes 77% 80% 74% p = .57
Child mental health problem
 Yes 27% 33% 22% p = .39
Parent mental health problem
 Yes 45% 52% 39% p = .36
IEPf use
 Yes 22% 23% 11% p = .027
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a

The Child Behavior Checklist (CBCL) is a standardized measure for problem behaviors and emotions with a mean t-score of 50 and a standard deviation of 10, with higher scores indicating more problem behaviors.

b

The Vineland Adaptive Behavior Scale includes three subdomains: communication, socialization, and daily living skills. The standardized mean score for this measure is 100, with a standard deviation of 15.

c

Child Cognition was measured using the NIH Toolbox Cognition Battery for Children. Parent cognition was measured using the Wechsler Adult Intelligence Scale. Both measures have a standardized mean score of 100, with a standard deviation of 15.

d

Pediatric Symptom Checklist (PSC), parent and youth reported. Scores ≥28 in parent reports require intervention, and scores ≥30 in youth reports require intervention.

e

The Parenting Styles and Dimensions (PSD) questionnaire assesses the degree a patient exhibits a specific parenting style, and is rated on a 5-point Likert scale. Higher scores reflect parenting behaviors and attitudes more indicative of the specified parenting style.

f

Individualized Education Plan (IEP)

Neurobehavioral outcomes of children

Due to Covid-19 and limitations of remote cognition testing, cognition scores were only available for 30 children. The mean level of neurocognitive functioning was below average for both children of parents with FASD (n=17, x̄=81.1, SD 13.0) and children of control parents (n=13, x̄=79.9, SD 16.1), with no between group differences. Vineland adaptive functioning was within the adequate range for both groups (x̄=92.4, SD 15.2 in FASD offspring and x̄=95.7, SD 14.6 in controls). Mean CBCLs in both groups were below the clinical range (x̄ =52.0, SD 12.4 in FASD offspring and x̄=50.3, SD 11.6 in controls) with low-average competency scores of x̄=42.9 and 42.0, respectively. Children were reportedly doing mostly well academically. No differences were found in neurocognitive or adaptive functioning or total competence scores between groups using 2-tailed t-test (p>0.05).

22% of parents with FASD reported at least 1 mental health problem in their child, compared to 33% of parents in the control group, with no differences between the groups. Reported family mental health problems were also similar in both groups. No differences were found in reported pediatric symptom checklist between groups and the difference between child and parent reported problems is not statistically significant. Table 2 summarizes the neurobehavioral outcomes of children.

Use of resources

Despite similar impairments in neurocognitive functioning in both groups, 38% of control-group children had an Individualized Education Plan per parent-report in contrast to only 11% of children of parents with FASD (χ2 (1, N = 48) =4.87, p<0.05). Use of other developmental and mental health resources was not statistically significant between groups. Table 2 summarizes the use of resources.

Trauma recognition

On average, children reported 7.2 experienced traumatic events and parents reported that the child experienced 4.4 traumatic events. The discrepancy between child- and parent-reported traumatic experiences was significantly different between the 2 groups: parents with FASD underrecognized 3.4 (SD=3.8) child-reported events and controls underrecognized 0.5 (SD=3.1) events (2-tailed t-test, p <0.05). Categorization of traumatic events into subtypes physical trauma, emotional trauma, witnessed violence, and sexual trauma or into subtypes interpersonal vs. non-interpersonal trauma did not uncover specific patterns in the type of trauma identified by parents vs. children.

Medical conditions

77% of all parents stated that their children had a medical condition, and 54% were actively taking medications. The most commonly reported medical conditions included asthma, allergies, epilepsy, and migraines. There were no differences in the frequency of reported medical conditions or use of medications between groups.

DISCUSSION

The first aim of this study was to investigate whether there are second-generation neurobehavioral effects of heavy prenatal alcohol exposure. To our knowledge, this is the first study to investigate the potential impact of prenatal alcohol exposure on the health of the offspring of individuals with FASD. As there is no systematic research on the multigenerational effects of prenatal alcohol exposure in humans, it is impossible to screen for, diagnose and treat potential effects on offspring in effective ways. Although anecdotal reports often speak of “breaking the cycle” of substance abuse and prenatal alcohol effects, we need knowledge about what this cycle embodies, and this study was designed to start addressing this gap in knowledge. In the current study, we examined offspring of parents with FASD and compared this group to offspring of socioeconomically matched, nonexposed control parents. Our hypothesis was that offspring of parents with FASD would have more impaired neurobehavioral functioning compared to offspring of control parents. We found that cognitive functioning was similarly impaired in both groups, and adaptive functioning and psychiatric symptomatology scores were reported to be within reference range in both groups.

One likely contributing factor for the low cognition scores in our sample is the low socioeconomic status (SES) of the sample. Indeed, a study by Hair et al. showed that childhood poverty is associated with atypical brain development and is linked with lower standardized test scores (Hair et al., 2015). In our sample, 37.5% of families lived under the federal poverty line, which is more than three times higher than the national average of 11.6% (Bureau, 2021). With a greater representation of subjects from low SES backgrounds in our study, it is likely this played a role in the lower cognition scores observed in both groups (von Stumm and Plomin, 2015). Despite similar impairments in intellectual development, children were reported to be doing mostly well academically in both groups. Although there is research that states that other factors may also play a significant role in academic performance, such as personality and self-perception, intellectual ability has long been the best predictor for academic achievement (Bergold and Steinmayr, 2018; Greven et al., 2009; Mayes et al., 2009). Since there should be a strong correlation between intellectual development and school performance, the performance expectations of the school systems of our cohort, serving mostly lower SES families, may not be aligned with the national average. Alternatively, parents may have been unaware of or underreporting academic difficulties.

We predicted that Vineland Adaptive Functioning and CBCL scores would be more impaired in offspring of parents with FASD. We did not find this effect, suggesting that adaptive deficits of FASD are not transmitted to the F2 generation. Variables such as family structure and support are important factors in the development of behavior and socialization, however, in our population, most children came from single family households, and family support scales showed limited support, thus family structure and support were unlikely to have contributed to the lack of observed impairments. A second possible explanation for the lack of observed differences, is underreporting of symptoms and deficits in the affected groups. As reported by Rutman and Van Bibber (Rutman and Van Bibber, 2010), a commonly observed theme in exposed parents was participants perception that their parenting ability was highly scrutinized, and that reaching out for help would lead to being viewed as high risk and needing further investigation by child welfare authorities. In addition to fears contributing to underreporting, underrecognition of deficits and needs may also lead to underreporting.

Indeed, parents with FASD reported fewer child-experienced traumatic events when compared to controls. Parents are known to have a difficult time recognizing trauma in their offspring; a study by Stover et. al, showed that agreement between parents and caregivers about the type of traumatic events experienced by the child and the impact of these events were poor, with youth reporting more events than parents (Stover et al., 2010). This effect appears to be magnified in parents with FASD, and a lack of recognition/reporting in this population can lead to reduced support and fewer services for children of adults affected by prenatal alcohol exposure.

Furthermore, it is important to note that the effects of discrepancies in the recognition of traumatic events in children’s lives may not present until later in life. Our sampling in childhood may be too early to detect a difference in psychiatric outcomes, and the risk of having a parent with FASD may not present until adulthood. This suggestion is supported by extensive research showing that adverse childhood events (ACEs) precipitate worse outcomes in depression, anxiety and quality of life in adults (Elmore and Crouch, 2020; Infrasca, 2003; Vederhus et al., 2021).

Lastly, sampling bias may have contributed in failure to detect differences in neurobehavioral outcomes between groups. Previous studies show that individuals with FASD are more likely to be incarcerated, have higher rates of premature deaths, and have higher rates of alcohol use disorder (Streissguth et al., 2004). Furthermore, mental health at midlife was recently studied in the cohort from which the parents in this study were recruited and the group prenatally exposed to alcohol had higher levels of depression, anxiety, bipolar disorder and ADHD than the nonexposed contrast group (Coles et al., 2022). Parent-child dyads affected by disrupted relationships, out-of-home placements/DCS involvement, law involvement/incarceration, parent mental illness, and/or homelessness, are less likely to be successfully recruited into our study. Our sample may therefore represent relatively more stable parent-child dyads with fewer neurobehavioral deficits.

The second goal of our study was to identify the characteristics and the challenges that parenting with FASD presented. Parents in the FASD group showed a trend towards having more alcohol use during their own pregnancy, which is a finding supported by Streissguth, et. al, who found that in adults with FASD, 46% experienced drug and alcohol problems (Streissguth et al., 2004). No differences in neurobehavioral deficits in offspring were seen, which may be attributed to the small sample size.

Despite similar impairments in intellectual development in both groups, children of parents with FASD were less likely to have an Individualized Education Plan. One possible explanation for this observed discrepancy is that neurocognitive impairments of FASD hinder the parent’s ability to recognize, and/or advocate for the deficiencies in their children. A study by Rehm et al. (2013) details the effectiveness of different advocacy styles of parents in addressing students’ special education needs, and highlights the importance of advocacy by parents. Recognition by systems of parental needs for support navigating systems to help recognize and advocate for special needs in their children may be lacking. As reported by Rutman and Van Bibber (2010), parents with FASD believed that social workers and other service providers perceived them as being unmotivated or unwilling to follow instructions rather than as having difficulty in understanding the instructions. Furthermore, parents with FASD may be less likely to ask for support for fear of being labeled as “unfit” parents. Parents with FASD described that child welfare policies prevented them from seeking support and resources unless they were viewed as being high risk of having their child apprehended or investigated by child welfare authorities (Rutman and Van Bibber, 2010). These perspectives highlight the need for systemic changes to promote equity and justice for marginalized families.

Although this study has highlighted some of the deficits due to FASD, our results also suggest notable strengths in parents with FASD. Parents with FASD reported a primarily authoritative parenting style which is the parenting style reported to be the most protective for child wellbeing (Monaghan et al., 2012). Indeed, the adequate adaptive functioning of the children, as well as normal CBCL and PSC scores may be indicative of the strengths and resilience displayed and transmitted by the parents in our cohort.

Limitations of our study include the use of questionnaires, which renders the data subject to recall bias and reporting bias, and academic and behavioral functioning could be validated by academic records. In addition, as discussed above, selection bias may have played a role on outcomes as more stable parent-child dyads are more likely to participate in a research study. Furthermore, because our study took place during the COVID-19 pandemic, some participants could only complete the remote parts of the assessment battery and were not able or willing to come in in-person for the NIH-toolbox cognitive assessment.

CONCLUSION

Data show FASD-offspring display below normal neurocognitive functioning, adequate adaptive functioning, and no excessive psychiatric symptomatology, similar to socio-economically matched controls. Despite similar neurocognitive deficits however, data show children of parents with FASD are less likely to receive academic supports through an Individualized Education Plan. Furthermore, parents with FASD underrecognize child trauma, both of which are likely to affect long-term outcomes negatively. Possible explanations for the observed group differences include known impairments in adaptive functioning in individuals affected by FASD which may translate into parent-child communication problems, lack of insight into neurobehavioral problems, and lack of advocacy skills. Transgenerational transmission of prenatal alcohol effects thus appears to occur at least through the mechanism of altered parental behaviors. Further research is needed to elucidate whether additional mechanisms, i.e. fetal programming effects on reproductive and/or gestational health, and/or (epigenetic) effects on the F1 germ cell either directly or through F1 somatic cell changes, also play a role. Our study highlights the need to identify and support parents with FASD to optimize their parenting abilities in the setting of their individual strengths and difficulties.

Source of Funding:

Funding for this study was provided by NIH/NIAAA Diversity Supplement 3U01AA026108-04S1A and the American Academy of Child and Adolescent Psychiatry Pilot Research Award for Junior Faculty and Child and Adolescent Psychiatry Fellows, supported by AACAP.

Footnotes

Conflicts of Interest: none

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