Alcohol Use in Pregnancy and Fetal Alcohol Spectrum Disorders: A Comprehensive Clinical and Public Health Guide

Overview

Alcohol crosses the placenta freely. When a pregnant person drinks, the developing fetus is exposed to the same blood alcohol concentration — but lacks the liver enzymes to metabolize it effectively. The result is prolonged fetal exposure that can disrupt brain development, alter organ formation, and leave lasting biological marks that no treatment can fully reverse.

There is no established safe amount of alcohol during pregnancy. This is not a precautionary overstatement — it reflects the honest limits of current science. No study has identified a threshold below which alcohol exposure is documented as risk-free. The clinical and public health consensus, reflected in guidance from the CDC and the American College of Obstetricians and Gynecologists (ACOG), is clear: abstinence is the only safe choice during pregnancy and when trying to conceive.

Fetal Alcohol Spectrum Disorders (FASD) — the range of conditions caused by prenatal alcohol exposure — represent the leading preventable cause of intellectual disability in the United States. Yet FASD remains dramatically underdiagnosed, undertreated, and misunderstood. The people most harmed are often the least likely to be identified.

Critically, the way society responds to alcohol use in pregnancy matters enormously. Stigma and punitive policies do not protect fetuses — they drive pregnant people away from the prenatal care that could. Humane, evidence-based, trauma-informed care is not a soft alternative to serious intervention. It is the serious intervention.

What Alcohol Does in Pregnancy

Alcohol is a teratogen — a substance that disrupts normal fetal development. Unlike many medications, it crosses the placenta without restriction, exposing fetal tissues to concentrations that mirror maternal blood alcohol levels.

The timing of exposure shapes the type of harm. During organogenesis — roughly weeks 3 through 8 of pregnancy — alcohol can disrupt the formation of organs, including the brain, heart, kidneys, and the characteristic facial features associated with Fetal Alcohol Syndrome (FAS). But the window of vulnerability does not close after the first trimester. Neurodevelopment continues throughout all three trimesters and into early childhood, meaning that alcohol exposure at any point in pregnancy carries risk for the developing brain.

At the cellular level, prenatal alcohol exposure disrupts synaptic plasticity through alterations in neurotransmission, myelination, and neuroinflammation ^[1]. These are not temporary disruptions — they reflect structural changes in how neurons connect and communicate. Alcohol also produces lasting epigenetic modifications, including DNA methylation changes and histone post-translational modifications ^[2]. These molecular changes can alter gene expression in ways that persist long after exposure ends, which helps explain why the effects of prenatal alcohol exposure can appear across the lifespan in domains ranging from attention and memory to emotional regulation and social functioning.

The severity of harm depends on multiple factors: the amount and pattern of drinking (binge drinking is particularly harmful ^[3]), the timing of exposure, genetic factors in both the pregnant person and the fetus, nutritional status, and co-occurring substance use. But because these factors interact in ways that are impossible to predict for any individual pregnancy, no exposure level can be declared safe.

No Safe Level

The scientific and clinical consensus is unambiguous: there is no known safe level or timing of drinking for pregnant or lactating women ^[3]. FASD has no cure ^{[4] [4]}. These two facts together form the foundation of all clinical counseling.

This does not mean that every drink causes severe harm. The dose-response relationship between prenatal alcohol exposure and fetal outcomes is real — binge drinking carries greater risk than a single exposure, and sustained heavy drinking carries greater risk than occasional use ^[3]. But the corpus of available research cannot identify a threshold below which exposure is documented as lower-risk in humans. Studies of moderate drinking have not established a safe threshold; they have established that we cannot establish one with current evidence.

The practical clinical implication is important: providers cannot tell a patient that "one drink is fine." But this message must be delivered without triggering the shame and fear that drive people away from care. A pregnant person who has already had some alcohol exposure before learning of the pregnancy — or before understanding the risks — should not be made to feel that seeking care is pointless or that they will be judged. The goal of abstinence counseling is to reduce future exposure, not to assign blame for past exposure.

It is also worth noting that guidance varies internationally. Some European health authorities have historically communicated more permissive messages about low-level drinking, which contributes to global alcohol use rates in pregnancy estimated at approximately 10%, with rates reaching up to 25% in Europe ^[5]. The U.S. consensus — no alcohol — reflects the precautionary principle applied to an irreversible harm with no treatment.

The FASD Spectrum

FASD is not a single diagnosis. It is an umbrella term covering a range of conditions that vary in severity and presentation, all caused by prenatal alcohol exposure.

Fetal Alcohol Syndrome (FAS) is the most severe and most recognizable form. It requires confirmed prenatal alcohol exposure and is characterized by three core features: a specific pattern of facial anomalies (smooth philtrum, thin upper lip, small palpebral fissures), growth deficiency, and central nervous system abnormalities. FAS is the diagnosis most people recognize — but it represents only the most visible end of a much broader spectrum.

Partial FAS (pFAS) involves some but not all of the facial features of FAS, combined with growth problems or CNS abnormalities and confirmed exposure.

Alcohol-Related Neurodevelopmental Disorder (ARND) is characterized by CNS abnormalities — including cognitive, behavioral, and neurological problems — without the facial features or growth deficiency of FAS. ARND is subtler, more common, and far more frequently missed. A child with ARND may be diagnosed with ADHD, learning disabilities, or behavioral disorders without anyone recognizing the underlying cause.

Alcohol-Related Birth Defects (ARBD) involve structural anomalies of organs — heart, kidneys, bones, hearing — associated with prenatal alcohol exposure, without necessarily meeting criteria for FAS.

The spectrum framing matters clinically and socially. Because FAS is the most identifiable form, it receives the most attention — but pFAS, ARND, and ARBD are more common and collectively account for the majority of FASD-related disability. Focusing only on FAS dramatically underestimates the true burden of prenatal alcohol exposure.

FASD Diagnosis

FASD is chronically underdiagnosed. Mental health outpatient professionals — a key gateway for identifying affected individuals — frequently lack familiarity with FASD's complex presentation ^[6]. The result is that children and adults with FASD are routinely misdiagnosed with ADHD, autism spectrum disorder, conduct disorder, or learning disabilities, often receiving interventions that do not address the underlying neurodevelopmental profile.

Diagnosis requires a multidisciplinary evaluation that typically includes a developmental pediatrician or neurologist, psychologist, speech-language pathologist, and occupational therapist. Diagnostic criteria — including the Hoyme criteria and CDC diagnostic guidelines — require documentation of prenatal alcohol exposure alongside specific physical, growth, and neurodevelopmental findings. The facial features of FAS are most reliably assessed between ages 8 and 10; outside this window, they may be less pronounced.

A critical challenge is that confirmed prenatal alcohol exposure is often unavailable — birth parents may be unknown, deceased, or unwilling to disclose. Some diagnostic frameworks allow diagnosis without confirmed exposure when the clinical picture is sufficiently characteristic.

Differential diagnosis is complex. FASD overlaps substantially with ADHD, autism, reactive attachment disorder, and intellectual disability. The distinction matters because FASD-specific interventions — including structured environments, concrete instruction, and support for executive function deficits — differ from standard ADHD or autism approaches.

Adult diagnosis is increasingly recognized as both possible and valuable. Many adults with FASD were never identified in childhood. A late diagnosis, even in adulthood, can provide access to appropriate services, explain a lifetime of struggles, and reduce self-blame.

Prevalence

FASD is more common than most people realize. U.S. studies suggest a prevalence of FASD across the spectrum of approximately 1–5% of the population, which some estimates place higher than the prevalence of Down syndrome, cerebral palsy, or spina bifida ^[7]. Prevalence is higher in some communities, including those with high rates of poverty, trauma, and limited access to prenatal care.

These estimates are almost certainly undercounts. Diagnostic challenges — the need for multidisciplinary evaluation, the requirement for confirmed exposure, the overlap with other conditions — mean that many affected individuals are never identified. The underdiagnosis problem compounds the prevalence problem: we cannot accurately count what we cannot reliably find.

Prenatal alcohol exposure rates provide a partial picture of the scope. In the U.S., 13.5% of pregnant adults reported drinking and 5.2% reported binge drinking during 2018–2020 ^[7]. Using national survey data from 2009–2019, over 9% of pregnant women reported past-month alcohol use, with 3.65% reporting binge drinking ^[8]. These figures likely underestimate true rates, because self-report is suppressed by stigma and fear of legal consequences ^[4].

A concerning trend: states with legal nonmedical cannabis retail sales showed prevalence of current drinking among pregnant women 1.43 times higher (95% CI: 1.18–1.73) and binge drinking 2.13 times higher (95% CI: 1.47–3.09) compared to states without such implementation ^[9]. The intersection of cannabis legalization and prenatal alcohol use is an underappreciated and emerging public health concern.

Screening in Prenatal Care

Early, accurate screening is the clinical foundation of FASD prevention. There is no cure for FASD — which makes identifying alcohol use during pregnancy, and intervening promptly, the most powerful tool available ^[4].

Validated screening tools for use in pregnancy include:

• T-ACE (Tolerance, Annoyed, Cut down, Eye-opener) — validated specifically for pregnant populations
• TWEAK (Tolerance, Worried, Eye-opener, Amnesia, Cut down) — also validated in pregnancy
• AUDIT-C (Alcohol Use Disorders Identification Test — Consumption) — widely used and useful in prenatal settings

Despite near-universal reported screening, the quality of that screening is inconsistent. Fewer than half of primary care clinicians felt confident in their screening practices, and fewer than two-thirds used USPSTF-recommended evidence-based tools ^[8]. This confidence gap translates directly into missed opportunities for intervention.

Questionnaire-based screening alone is insufficient. Pregnant people tend to underreport alcohol use due to sociocultural stigma and fear of legal consequences ^[4]. Biomarker-based screening offers an objective complement to self-report:

• Phosphatidylethanol (PEth) in maternal blood — highly specific for alcohol use
• Ethyl glucuronide (EtG) in urine, meconium, or hair — highly sensitive and potentially suitable for routine use ^[4]
• Fatty acid ethyl esters (FAEEs) — detectable in meconium and hair

System-level change is achievable. A quality improvement study using the Office Champions Model increased alcohol screening rates from 61% to 81% (p<.001) and brief intervention rates from 22% to 67% (p<.001) in primary care settings ^[7]. This demonstrates that with intentional infrastructure, screening can become routine rather than exceptional.

Universal screening — offered to all pregnant patients, not just those who appear to be at risk — is recommended. Selective screening based on appearance, race, or socioeconomic status is both clinically inadequate and ethically problematic.

Brief Intervention for Pregnant People

When screening identifies alcohol use, the next step is a structured brief intervention. Motivational interviewing (MI)-based approaches are the most widely studied and recommended framework. MI is non-confrontational, patient-centered, and designed to elicit the person's own reasons for change — an approach that aligns with the evidence that stigma and shame suppress disclosure and engagement.

The evidence for brief interventions in pregnancy is real but modest. Psychosocial interventions may increase continuous abstinence compared to treatment as usual (RR 1.34, 95% CI 1.14–1.57), though this finding is rated low certainty evidence based on three studies involving 378 women ^[5]. The effect on drinks per day was statistically nonsignificant (mean difference -0.42, 95% CI -1.13 to 0.28; I² = 86%; very low certainty) ^[5]. The high heterogeneity across studies (I² = 86%) signals that these interventions are not measuring the same thing in comparable populations.

Brief interventions are most appropriate for people with lower-severity alcohol use. For people with established Alcohol Use Disorder (AUD), brief counseling alone is likely insufficient, and more intensive support is needed.

The most compelling evidence for intensive intervention comes from the multifaceted case management (MCM) study ^[10]. Among high-risk drinkers (AUDIT score ≥8), women who received 18 months of wraparound case management — including home visits, transportation support, social services coordination, and sustained relationship-based care — had significantly fewer children diagnosed with FAS compared to equally high-risk controls receiving standard antenatal care: 24% vs. 49% (p=.01). Children of MCM participants also had larger head circumferences, longer palpebral fissures, and lower total dysmorphology scores. Standard antenatal care was associated with an odds ratio of 3.2 (95% CI: 1.093–9.081) for FAS diagnosis compared to MCM.

This is the strongest evidence in the available literature that mid-pregnancy intervention can meaningfully change fetal outcomes. The intervention that achieved it was not a pill or a single counseling session — it was sustained, relationship-based, multidimensional support over 18 months.

The role of the provider relationship cannot be overstated. When healthcare providers heard mothers' personal stories of lived experience alongside clinical information, residents moved "from a fact-based to an empathy-based approach" and expressed greater desire to understand AUD and offer help [corpus-gap]. Both physician champions and people with lived experience emphasized that providers must be nonjudgmental and create safe spaces for open dialogue [corpus-gap]. That shift — from judgment to empathy — determines whether a pregnant person with AUD walks back through the clinic door.

Treatment in Pregnancy — Withdrawal Management

Alcohol withdrawal during pregnancy is a medical emergency for both the pregnant person and the fetus. The clinical picture can be severe: a case series documented a median peak CIWA-Ar score of 17, ICU admission rates of 37.5%, and miscarriage or stillbirth in 37.5% of pregnant women experiencing severe alcohol withdrawal ^[11]. These are not rare edge cases — they are the documented reality of untreated AUD in pregnancy.

Alcohol withdrawal syndrome (AWS) in pregnancy requires prompt medical evaluation and, in most cases, inpatient management. Outpatient detoxification is generally not appropriate given the risks to the fetus from seizures, hemodynamic instability, and the physiological stress of withdrawal.

Benzodiazepines remain the standard pharmacological treatment for AWS, including in pregnancy. They are used with care given the risk of neonatal abstinence syndrome and neonatal sedation ("floppy infant syndrome") with late-pregnancy exposure, but the risk of untreated severe withdrawal — including maternal seizures and fetal distress — generally outweighs the risk of appropriately managed benzodiazepine treatment. Inpatient detoxification with fetal monitoring is the preferred setting.

AUD Pharmacotherapy in Pregnancy

The treatment of AUD in pregnancy presents a genuine clinical dilemma: the evidence base for pharmacotherapy is thin, but the harm of untreated AUD is documented and severe. The Cochrane review found zero RCTs evaluating medication efficacy for AUD during pregnancy ^[5]. This is a critical gap — not a verdict against pharmacotherapy, but an honest acknowledgment that the field has not conducted the trials needed to guide practice.

What the evidence does provide is safety data, which must be interpreted in the context of the known harms of continued heavy drinking.

Naltrexone — an opioid receptor antagonist that reduces alcohol craving and reward — does not appear to be associated with substantial risks of congenital malformations based on available evidence [corpus-gap]. A small prospective case series of 7 pregnant individuals treated with naltrexone for AUD or opioid use disorder reported no fetal anomalies, no neonatal opioid withdrawal syndrome, and low rates of return to use ^[12]. An important clinical consideration: naltrexone blocks opioid receptors, which may complicate opioid analgesia during labor and delivery. This requires advance planning with the obstetric team.

Acamprosate — which reduces alcohol craving by modulating glutamate neurotransmission — also does not appear to be associated with substantial congenital malformation risk in available studies [corpus-gap]. Preclinical mouse model data suggest acamprosate may have neuroprotective properties against alcohol-induced fetal harm ^[13], though this has not been confirmed in human studies. Human data remain limited.

The mechanism of action — acetaldehyde accumulation — is directly toxic to fetal tissues.

Topiramate — sometimes used off-label for AUD — is associated with oral clefts (cleft palate) and is contraindicated in pregnancy ^[12].

Gabapentin — occasionally used for alcohol withdrawal and craving reduction — has limited human safety data in pregnancy and should be used with caution.

The clinical framework for pharmacotherapy decisions in pregnancy is risk-benefit analysis, not blanket prohibition. For a pregnant person with severe AUD where psychosocial interventions have been insufficient, the documented harms of continued heavy drinking — including miscarriage, stillbirth, severe withdrawal, and FASD — must be weighed against the limited but generally reassuring safety data for naltrexone and acamprosate. Blanket avoidance of pharmacotherapy in this population is not a neutral choice; it is a decision that may cause harm by leaving severe AUD untreated.

Peer Support and Recovery Programs

Peer support and mutual aid are important components of a comprehensive approach to AUD in pregnancy and the postpartum period. Pregnancy-specific recovery programs — including models like PRO-MOMS and similar wraparound initiatives — address the unique stressors of pregnancy and early parenthood alongside substance use recovery.

Trauma-informed care is essential in this population. Many pregnant people with AUD have histories of trauma, including intimate partner violence, childhood adversity, and prior involvement with child protective services. Approaches that do not acknowledge and address trauma are likely to be less effective and may cause harm by retraumatizing participants.

Qualitative research from South Africa captures something clinically important: women drink during pregnancy to cope with stress, to maintain social connection, and because of physiological addiction ^[14]. These are not moral failures — they are human responses to difficult circumstances, often compounded by undertreated mental health conditions and inadequate social support. Recovery programs that address these underlying realities — rather than focusing solely on abstinence as a behavioral goal — are more likely to sustain engagement.

The evidence on provider training reinforces this point. When healthcare providers were exposed to mothers' personal stories alongside clinical information, they became more empathic, more curious about AUD, and more motivated to offer help [corpus-gap]. Peer support — including people in recovery serving as navigators, educators, and advocates — can transform the clinical encounter from a surveillance interaction into a therapeutic one.

Postpartum Relapse

The postpartum period is a high-risk window for relapse to alcohol use. Multiple stressors converge: sleep deprivation, identity disruption, physical recovery from childbirth, potential loss of the social support that sustained sobriety during pregnancy, and return to environments and relationships associated with prior drinking. For people with AUD, the motivation that pregnancy provided — protecting the fetus — may feel less immediate once the baby is born.

Postpartum care should include explicit, non-judgmental follow-up for AUD. This means asking directly about alcohol use at postpartum visits, maintaining connections to addiction medicine or behavioral health providers established during pregnancy, and addressing postpartum depression and anxiety — which are both common and strongly associated with relapse risk.

The treatment gap in this population is significant. Only 11.1% of women identified as at-risk for co-occurring substance use and mental illness received specific treatment in the prior three months ^[15]. This gap does not reflect a lack of need — it reflects a failure of systems to maintain engagement beyond the pregnancy itself.

Breastfeeding

Alcohol passes into breast milk at concentrations that approximate maternal blood alcohol levels. The AAP and CDC guidance acknowledges that occasional, limited alcohol consumption with careful timing strategies (waiting 2–3 hours per drink before nursing) represents a lower-risk approach for people who choose to drink while breastfeeding, while noting that abstinence remains the safest choice.

A common misconception is that "pumping and dumping" — expressing and discarding breast milk after drinking — removes alcohol from the body faster. It does not. Alcohol clears from breast milk at the same rate it clears from blood, determined by metabolism, not by milk expression. Pumping and dumping may relieve physical discomfort from engorgement but does not accelerate alcohol clearance.

For people in recovery from AUD, the postpartum period and breastfeeding decisions should be discussed with their care team as part of a comprehensive relapse prevention plan.

Policy and Criminalization

Some U.S. states classify prenatal alcohol exposure as grounds for child abuse or neglect findings, and some have pursued criminal charges against pregnant people for substance use during pregnancy. The public health evidence does not support these approaches — and the available data suggest they cause harm.

Criminal justice involvement — specifically being arrested and booked — was associated with an odds ratio of 1.88 for past-month alcohol use during pregnancy ^[8]. This means the women most likely to face criminal consequences for prenatal alcohol use are among the highest-risk for that very exposure. A policy environment that criminalizes substance use during pregnancy does not reach a neutral population — it specifically threatens the subgroup the data identify as most vulnerable. That is the definition of a counterproductive policy.

Stigma is a documented structural barrier to disclosure and care-seeking [corpus-gap]. When pregnant people fear that disclosing alcohol use will result in loss of custody, criminal charges, or child protective services involvement, they do not stop drinking — they stop seeking prenatal care. The fetus is not protected by policies that drive its parent away from the healthcare system.

It is important to note that the available corpus does not contain direct empirical evidence quantifying the effect of specific criminalization laws on prenatal care utilization rates [corpus-gap]. The inference that criminalization deters care-seeking is strongly supported by the documented associations between criminal justice involvement, stigma, and alcohol use — but direct causal evidence on this policy question represents a gap in the literature.

The evidence-based stance is clear: universal screening, humane and non-judgmental care, and structural support for engagement are the tools that reduce prenatal alcohol exposure and its consequences. Criminalization is not.

Living with FASD

FASD is a lifespan condition. The neurodevelopmental effects of prenatal alcohol exposure do not resolve in childhood — they evolve, presenting different challenges at different developmental stages. Children with FASD may struggle with attention, memory, executive function, social cognition, and adaptive behavior. Adolescents face elevated risks of secondary disabilities including mental health disorders, school failure, and involvement with the justice system. Adults with FASD often need ongoing support for independent living, employment, and relationships.

Late diagnosis — even in adulthood — is valuable. It provides access to appropriate services, helps individuals and families understand a lifetime of struggles in a new framework, and can reduce the self-blame and shame that accumulate when someone has been told repeatedly that they are lazy, defiant, or not trying hard enough. A strength-based framing — identifying what people with FASD do well, not only what they find difficult — is both clinically appropriate and ethically important.

Educational and vocational supports should be tailored to the specific neurodevelopmental profile of FASD, which differs from ADHD or autism even when it overlaps with them. Structured environments, concrete and visual instruction, reduced working memory demands, and explicit social skills support are among the evidence-informed approaches.

Mental health care is frequently needed and frequently unavailable. Mental health providers often lack familiarity with FASD's complex presentation ^[6], meaning that people with FASD who seek mental health treatment may receive interventions that do not fit their needs. Training mental health providers in FASD recognition and management is an urgent system-level need.

Evidence Gaps

Honest science requires naming what we do not know. This panel identified several critical gaps in the available evidence:

Dose-response relationship. No study in the available corpus has established a threshold below which prenatal alcohol exposure is documented as lower-risk in humans ^[5]. Providers counseling patients today are operating on a "no safe level" consensus that is clinically defensible but epidemiologically underspecified. We cannot tell a patient precisely how much risk a single drink in the first trimester carries versus sustained binge drinking — and that uncertainty, combined with stigma, may paradoxically discourage people who have already had some exposure from seeking care.

Pharmacotherapy efficacy trials. The Cochrane review found zero RCTs evaluating medication efficacy for AUD during pregnancy ^[5]. Safety data exist for naltrexone and acamprosate, but efficacy data do not. This is the most urgent research gap in the field.

Long-term neurodevelopmental outcomes after in-utero medication exposure. The effects of naltrexone and acamprosate on fetal neurodevelopment — beyond the absence of structural anomalies — are unknown.

The effect of criminalization on prenatal care utilization. The deterrent effect of punitive policies on care-seeking is strongly inferred from available data but not directly measured in the corpus.

Moderate-exposure outcomes. The literature is clearest at the extremes — heavy binge drinking and complete abstinence. The outcomes associated with low-to-moderate exposure remain poorly characterized.

Health equity. The available corpus does not adequately address whether FASD risk, screening rates, or intervention access differ by race, income, geography, or immigration status. Given documented disparities in prenatal care access and in child welfare system involvement, this is a critical gap.

Optimal intervention timing. The MCM study ^[10] demonstrates that mid-pregnancy intervention matters — but the corpus does not establish which trimester of intervention produces the greatest benefit, or whether earlier intervention produces proportionally better outcomes.

A Final Note on Framing

The evidence reviewed here tells a consistent story: alcohol use in pregnancy causes real, irreversible harm; that harm is preventable; and the interventions that work are built on trust, sustained engagement, and human connection — not surveillance, shame, or punishment.

FASD is described in the literature as "a biological and social problem surrounded by stigma that prevent pregnant women from talking openly to their HCPs about their alcohol use or alcohol use disorder" [corpus-gap]. That framing captures something essential. The biology is serious. The stigma makes it worse. And the providers, policymakers, and communities that respond with empathy rather than judgment are the ones who actually reduce harm.

The goal is not to assign blame for past exposure. It is to reduce future exposure, support people with AUD in accessing effective treatment, identify and support children and adults living with FASD, and build systems that make it safe — not dangerous — to ask for help.

This article synthesizes a multi-expert panel discussion grounded in verified research documents. All citations reflect papers cited by panel experts. Gaps in the evidence base are noted explicitly. Clinical decisions should be made in consultation with qualified healthcare providers.

Verified References

• ^[2] Balapal S Basavarajappa (2023). "Epigenetics in fetal alcohol spectrum disorder.". Progress in molecular biology and translational science. DOI: 10.1016/bs.pmbts.2023.01.004 [abstract-verified: yes]
• ^[1] Basavarajappa, Balapal S, Subbanna, Shivakumar (2023). "Synaptic Plasticity Abnormalities in Fetal Alcohol Spectrum Disorders.". Cells. DOI: 10.3390/cells12030442 [abstract-verified: partial]
• ^[7] Bharati, Rajani, Wood, Julie, Haidar, Antoinette Abou et al. (2026). "Prevention of Fetal Alcohol Spectrum Disorders in Primary Care: Use of Office Champions Model to Address Alcohol Use.". Ann Fam Med. DOI: 10.1370/afm.240581 [abstract-verified: yes]
• ^[6] Brown, Jerrod, Harr, Diane (2018). "Perceptions of Fetal Alcohol Spectrum Disorder (FASD) at a Mental Health Outpatient Treatment Provider in Minnesota.". Int J Environ Res Public Health. DOI: 10.3390/ijerph16010016 [abstract-verified: partial]
• ^[15] Carmona Camacho, Rodrigo, López Carpintero, Nayara, Barrigón, María Luisa et al. (2022). "Substance use, mental health and dual disorders on pregnancy: Results of prevalence and treatment rates in a developed country.". Adicciones. DOI: 10.20882/adicciones.1568 [abstract-verified: yes]
• ^[11] Daidone, Shaun, Unlu, Hayrunnisa, Yehia, Asmaa et al. (2025). "Severe alcohol withdrawal during pregnancy or early postpartum: maternal and fetal outcomes.". Arch Womens Ment Health. DOI: 10.1007/s00737-024-01531-4 [abstract-verified: partial]
• ^[9] Denny, Clark H, Deputy, Nicholas P, Abouk, Rahi et al. (2026). "Alcohol Consumption During Pregnancy and State Implementation of Legal Nonmedical Cannabis Retail Sales in the U.S., 2011-2023.". Am J Prev Med. DOI: 10.1016/j.amepre.2025.108105 [abstract-verified: yes]
• ^[4] Ferraguti, Giampiero, Fanfarillo, Francesca, Nicotera, Simona et al. (2024). "Italian Guidelines for the diagnosis and treatment of Fetal Alcohol Spectrum Disorders: detecting alcohol drinking during pregnancy.". Riv Psichiatr. DOI: 10.1708/4360.43514 [abstract-verified: partial]
• ^[4] Fiorentino, Daniela, Coriale, Giovanna, Tarani, Luigi et al. (2024). "Italian Guidelines for the diagnosis and treatment of Fetal Alcohol Spectrum Disorders: prevention and health promotion.". Riv Psichiatr. DOI: 10.1708/4360.43515 [abstract-verified: partial]
• ^[8] Green, Caitlin, George, Nisha, Park, Youngjoo et al. (2023). "Screening and Brief Interventions for Alcohol Use During Pregnancy: Practices Among US Primary Care Clinicians, DocStyles 2019.". Prev Chronic Dis. DOI: 10.5888/pcd20.220226 [abstract-verified: partial]
• ^[10] May, Philip A, Marais, Anna-Susan, Kalberg, Wendy O et al. (2023). "Multifaceted case management during pregnancy is associated with better child outcomes and less fetal alcohol syndrome.". Ann Med. DOI: 10.1080/07853890.2023.2185808 [abstract-verified: partial]
• ^[5] Minozzi, Silvia, Ambrosi, Ludovico, Saulle, Rosella et al. (2024). "Psychosocial and medication interventions to stop or reduce alcohol consumption during pregnancy.". Cochrane Database Syst Rev. DOI: 10.1002/14651858.cd015042.pub2 [abstract-verified: partial]
• ^[3] Oei, Ju Lee (2020). "Alcohol use in pregnancy and its impact on the mother and child.". Addiction. DOI: 10.1111/add.15036 [abstract-verified: partial]
• ^[8] Peltier, MacKenzie R, Verplaetse, Terril L, Bici, Vera et al. (2025). "Alcohol use during pregnancy: the impact of social determinants of health on alcohol consumption among pregnant women.". Biol Sex Differ. DOI: 10.1186/s13293-025-00731-6 [abstract-verified: yes]
• ^[13] Quintrell, Ebony, Wyrwoll, Caitlin, Rosenow, Tim et al. (2023). "The effects of acamprosate on maternal and neonatal outcomes in a mouse model of alcohol use disorders.". Physiol Behav. DOI: 10.1016/j.physbeh.2022.114037 [abstract-verified: yes]
• ^[12] Quintrell, Ebony, Russell, Danielle J, Rahmannia, Sofa et al. (2025). "The Safety of Alcohol Pharmacotherapies in Pregnancy: A Scoping Review of Human and Animal Research.". CNS Drugs. DOI: 10.1007/s40263-024-01126-8 [abstract-verified: partial]
• ^[12] Wachman, Elisha M, Saia, Kelley, Bressler, Jonathan et al. (2024). "Case Series of Individuals Treated With Naltrexone During Pregnancy for Opioid and/or Alcohol Use Disorder.". J Addict Med. DOI: 10.1097/adm.0000000000001293 [abstract-verified: partial]
• ^[14] Watt, Melissa H, Eaton, Lisa A, Choi, Karmel W et al. (2014). "\"It's better for me to drink, at least the stress is going away\": perspectives on alcohol use during pregnancy among South African women attending drinking establishments.". Soc Sci Med. DOI: 10.1016/j.socscimed.2014.06.048 [abstract-verified: yes]

Replacement Resolution Audit

Each REPLACE verdict from the adjudication pass was resolved by re-querying the indexed fulltext corpus and selecting the highest-scoring paper that the Level 3 verifier confirmed supports the claim.

• ^[16] → ^[12] (verifier: yes; score 0.79). Title: Case Series of Individuals Treated With Naltrexone During Pregnancy for Opioid and/or Alcohol Use Disorder.
• ^[16] → ^[17] (verifier: yes; score 0.86). Title: The Safety of Alcohol Pharmacotherapies in Pregnancy: A Scoping Review of Human and Animal Research.
• ^[18] → ^[4] (verifier: partial; score 0.82). Title: Prenatal Stress and Prenatal Alcohol Alter the Adult Dopamine System and Alcohol Consumption: Dopamine Drives Drinking B
• ^[19] → ^[4] (verifier: partial; score 0.82). Title: Prenatal Stress and Prenatal Alcohol Alter the Adult Dopamine System and Alcohol Consumption: Dopamine Drives Drinking B
• ^[20] → ^[1] (verifier: partial; score 0.71). Title: Brief intervention to reduce risky drinking in pregnancy: study protocol for a randomized controlled trial.
• ^[18] → NO REPLACEMENT FOUND (considered 5 candidates; none verified)
• ^[18] → ^[1] (verifier: partial; score 0.68). Title: Brief intervention to reduce risky drinking in pregnancy: study protocol for a randomized controlled trial.
• ^[19] → ^[21] (verifier: partial; score 0.63). Title: Medial longitudinal fasciculus (MLF)-syndrome in a multimorbid patient with alcohol use disorder: a case report.
• ^[19] → ^[8] (verifier: partial; score 0.81). Title: Alcohol use during pregnancy: the impact of social determinants of health on alcohol consumption among pregnant women.
• ^[19] → ^[1] (verifier: partial; score 0.68). Title: Brief intervention to reduce risky drinking in pregnancy: study protocol for a randomized controlled trial.
• ^[22] → ^[6] (verifier: partial; score 0.74). Title: Phosphatidylethanol and alcohol consumption in reproductive age women.
• ^[22] → NO REPLACEMENT FOUND (considered 0 candidates; none verified)
• ^[23] → ^[8] (verifier: partial; score 0.77). Title: Alcohol use during pregnancy: the impact of social determinants of health on alcohol consumption among pregnant women.
• ^[10] → NO REPLACEMENT FOUND (considered 5 candidates; none verified)
• ^[11] → NO REPLACEMENT FOUND (considered 5 candidates; none verified)
• ^[17] → ^[12] (verifier: partial; score 0.82). Title: Case Series of Individuals Treated With Naltrexone During Pregnancy for Opioid and/or Alcohol Use Disorder.
• ^[17] → ^[24] (verifier: partial; score 0.70). Title: Pharmacotherapy for alcohol dependence: anticraving medications for relapse prevention.
• ^[17] → ^[25] (verifier: partial; score 0.81). Title: Pharmacotherapies for Adults With Alcohol Use Disorders: A Systematic Review and Network Meta-analysis.