Jump to content

Fetal alcohol spectrum disorder

From Wikipedia, the free encyclopedia
(Redirected from Fetal alcohol syndrome)

Fetal alcohol spectrum disorders
Other namesFoetal alcohol spectrum disorders, FASD
Baby with fetal alcohol syndrome, showing some of the characteristic facial features
SpecialtyEmbryology, toxicology, psychiatry, neurology, gynaecology, obstetrics, neonatology, pediatrics
SymptomsVaried; Abnormal appearance, short height, low body weight, small head size, poor coordination, behavior problems similar to ADHD, learning and speech problems, Intellectual disability[1][2]
Usual onsetPrenatal
TypesFetal alcohol syndrome, partial fetal alcohol syndrome, alcohol-related neurodevelopmental disorder, static encephalopathy, alcohol-related birth defects[1]
CausesDrinking alcohol during pregnancy[1]
Diagnostic methodBased on symptoms and prenatal alcohol exposure[1]
Differential diagnosisADHD, autism, bipolar disorder, conduct disorder, learning disability, oppositional defiant disorder
PreventionAvoiding drinking alcohol during pregnancy[4]
TreatmentParent-child interaction therapy, efforts to modify child behavior, possibly medications[5]
PrognosisAverage life expectancy at death 34 years old (FAS).[6]
Unconfirmed (other types)
FrequencyUnconfirmed; between 1 in 20 (~390 million)[7] and 1 in 13 (~600 million) (all types)[8]
0.2 and 9 per 1,000 (FAS)

Fetal alcohol spectrum disorders (FASDs) are a group of conditions that can occur in a person who is exposed to alcohol during gestation, as a result of their mother drinking alcohol during pregnancy.[1] The several forms of the condition (in order of most severe to least severe) are: fetal alcohol syndrome (FAS), partial fetal alcohol syndrome (pFAS), alcohol-related neurodevelopmental disorder (ARND),[1] and neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE).[9] Other terms used are fetal alcohol effects (FAE), partial fetal alcohol effects (PFAE), alcohol-related birth defects (ARBD),[1][10] and static encephalopathy,[11] but these terms have fallen out of favor and are no longer considered part of the spectrum.[12]

Not all infants exposed to alcohol in utero will have detectable FASD or pregnancy complications. The risk of FASD increases with amount consumed, the frequency of consumption, and longer duration of alcohol consumption during pregnancy, particularly binge drinking. The variance seen in outcomes of alcohol consumption during pregnancy is poorly understood. Diagnosis is based on an assessment of growth, facial features, central nervous system, and alcohol exposure by a multi-disciplinary team of professionals. The main criteria for diagnosis of FASD is nervous system damage and alcohol exposure, with FAS including congenital malformations of the lips and growth deficiency. FASD is often misdiagnosed as or comorbid with ADHD.

Almost all experts recommend that the mother abstain from alcohol use during pregnancy to prevent FASDs. As the woman may not become aware that she has conceived until several weeks into the pregnancy, it is also recommended to abstain while attempting to become pregnant. Although the condition has no known cure, treatment can improve outcomes. Treatment needs vary but include psychoactive medications, behavioral interventions, tailored accommodations, case management, and public resources. Globally, one in 10 women drink alcohol during pregnancy, and the prevalence of having any FASD disorder is estimated to be at least 1 in 20. The rates of alcohol use, FAS, and FASD are likely to be underestimated, because of the difficulty in making the diagnosis and the reluctance of clinicians to label children and mothers. Some have argued that the FAS label stigmatizes alcohol use, while authorities point out that the risk is real. The condition has appeared in several works of fiction.

Signs and symptoms[edit]

Facial characteristics of a child with FAS

The key signs of fetal alcohol syndrome (FAS) required for diagnosis include:

Popova et al. identified 428 ICD-10 conditions as co-occurring in individuals with FAS. Excluding conditions used in FAS diagnosis, co-occurring conditions with 50% prevalence or greater include:[15]

Other FASD conditions are partial expressions of FAS where the central nervous system shows clinical deficits. In these other FASD conditions, an individual may be at greater risk for adverse outcomes because brain damage is present without associated visual cues of poor growth or the "FAS face" that might ordinarily trigger an FASD evaluation. Such individuals may be misdiagnosed with primary mental health disorders such as ADHD or oppositional defiance disorder without appreciation that brain damage is the underlying cause of these disorders, which requires a different treatment paradigm than typical mental health disorders. While other FASD conditions may not yet be included as an ICD or DSM-IV-TR diagnosis, they nonetheless pose significant impairment in functional behavior because of underlying brain damage.[citation needed] Many indications of fetal alcohol spectrum disorders are developmental. Therefore, although a child may appear 'normal' at birth, intellectual disabilities caused by alcohol before birth may not appear until the child begins school.[16]

More broadly, alcohol use during pregnancy is also associated with:[1][17]

Alcohol can also harm the fertility of women who are planning for pregnancy. Adverse effects of alcohol can lead to malnutrition, seizures, vomiting and dehydration. The mother can suffer from anxiety and depression which can result in child abuse/neglect. It has also been observed that when the pregnant mother withdraws from alcohol, its effects are visible on the infant as well. The baby remains in an irritated mood, cries frequently, doesn't sleep properly, weakening of sucking ability and increased hunger.[24]

In 2019, a study found that individuals with FASD have a higher risk of hypertension independent of race/ethnicity and obesity.[25]



Fetal alcohol syndrome 1) Alcohol consumed (EtOH) 2) Alcohol crosses into the placenta 3) Alcohol metabolizes 4) Fatty acid ethyl esters (FAEE) detected in meconium

Fetal alcohol spectrum disorders are caused by the mother's drinking alcohol while pregnant with the affected person;[1] if an individual was not exposed to alcohol before birth, they will not get FASD.[26] However, not all infants exposed to alcohol in utero will have detectable FAS, FASD, or pregnancy complications. Drinking any quantity during pregnancy, the risk of giving birth to a child with FASD is about 15%, and to a child with FAS about 1.5%. Drinking large quantities, defined as 2 standard drinks a day, or 6 standard drinks in a short time, carries a 4.3% risk of a FAS birth (i.e. one of every 23 heavy-drinking pregnant women will deliver a child with FAS). Furthermore, alcohol-related congenital abnormalities occur at an incidence of roughly one out of 67 women who drink alcohol during pregnancy.[27] Among those mothers who are alcoholic, an estimated one-third of their children have FAS.[28]

The risk of FASD increases with amount consumed, the frequency of consumption, and longer duration of alcohol consumption during pregnancy.[29][30][31] Blood alcohol concentration has been identified as a relevant factor.[32] All forms of alcohol, such as beer, wine, and liquor, pose similar risk.[33] Binge drinking increases the chances and severity of FASD to such an extent that Svetlana Popova has stated that "binge drinking is the direct cause of FAS or FASD".[34]

Evidence regarding the effects of low levels of alcohol consumption during pregnancy is inconsistent and contradictory: many studies find no significant effect, but some find beneficial associations, and others find detrimental associations, even on the same outcomes. Summarizing studies by country shows some similarity in results, due to using the same data source. The definition of low alcohol consumption varies significantly among studies and often fails to incorporate all aspects of timing, dose, and duration. Recall bias and socioeconomic and psychosocial factors have been controlled for in most studies, but it is likely that residual confounding due to missing factors and variation in methods still exists and is larger than any observed effects.[35][36][28][37][21] Because alcohol is a known teratogen, it is considered unethical to do randomized controlled trials on pregnant women to determine the precise level of alcohol toxicity,[38] so studies mainly rely on observational evidence.[17] Small amounts of alcohol may not cause an abnormal appearance, however, small amounts of alcohol consumption while pregnant may cause behavioral problems and also increases the risk of miscarriage.[39][28][40][41][42] Quasi-experimental studies provide moderately strong evidence that prenatal alcohol exposure causes detrimental cognitive outcomes, and some evidence of reduced birthweight, although no study was fully rated at low risk of bias and quantity of studies was limited.[43]

The variance seen in outcomes of alcohol consumption during pregnancy is poorly understood. Aggravating factors may include advanced maternal age, smoking, poor diet,[44][30] genetics, and social risk factors.[29]


Fathers who consume alcohol prior to conception may contribute to FAS through long term epigenetic modification of the father's sperm.[28][45]


After the mother consumes alcohol, the alcohol crosses through the placenta and umbilical cord to the developing fetus. Alcohol metabolizes slowly in the fetus and remains for a long time when compared to an adult.[46][32] A human fetus appears to be at triple risk from maternal alcohol consumption:[47][48]

  1. The placenta allows free entry of ethanol and toxic metabolites like acetaldehyde into the fetal compartment. The so-called placental barrier is practically absent with respect to ethanol.
  2. The developing fetal nervous system appears particularly sensitive to ethanol toxicity. The latter interferes with proliferation, differentiation, neuronal migration, axonic outgrowth, integration, and fine-tuning of the synaptic network. In short, all major processes in the developing central nervous system appear compromised.
  3. Fetal tissues are quite different from adult tissues in function and purpose. For example, the main detoxicating organ in adults is the liver, whereas the fetal liver is incapable of detoxifying ethanol, as the ADH and ALDH enzymes have not yet been brought to expression at this early stage. Up to term, fetal tissues do not have significant capacity for the detoxification of ethanol, and the fetus remains exposed to ethanol in the amniotic fluid for periods far longer than the decay time of ethanol in the maternal circulation. The lack of significant quantities of ADH and ALDH means that fetal tissues have much lower quantities of antioxidant enzymes, like SOD, glutathione transferases, and glutathione peroxidases, resulting in antioxidant protection being much less effective.

Although alcohol is known to be a teratogen (causing birth defects), the exact biological mechanisms for the development of FAS or FASD are unknown. However, clinical and animal studies have identified a broad spectrum of pathways through which maternal alcohol can negatively affect the outcome of a pregnancy. Clear conclusions with universal validity are difficult to draw, since different ethnic groups show considerable genetic polymorphism for the hepatic enzymes responsible for ethanol detoxification.[49] Genetic examinations have revealed a continuum of long-lasting molecular effects that are not only timing specific but are also dosage specific; with even moderate amounts being able to cause alterations.[50] Additionally, ethanol may alter fetal development by interfering with retinoic acid signaling as acetaldehyde can compete with retinaldehyde and prevents its oxidation to retinoic acid.[51]

Developmental stages[edit]

Different body systems in the infant grow, mature and develop at specific times during gestation. The effect of consumption of alcohol differs during each of these developmental stages:[16]

  • From conception and to the third week, the most susceptible systems and organs are the brain, spinal cord, and heart. The effects of alcohol consumption early in the pregnancy can result in defects to these systems and organs.[16]
  • During the third week, alcohol can also damage the central nervous system of the fetus.[52]
  • During the fourth week of gestation, the limbs are being formed and it is at this point that alcohol can affect the development of arms, legs, fingers and toes. The eyes and ears also form during the fourth week and are more susceptible to the effects of alcohol.[16]
  • By the sixth week of gestation, the teeth and palate are forming and alcohol consumption at this time will affect these structures. Alcohol use in this window is responsible for many of the facial characteristics of fetal alcohol syndrome.[16]
  • During the twelfth week, frequent alcohol exposure can negatively impact the brain development which affects cognitive, learning and behavioral skills before birth.[52]
  • By the 20th week of gestation the formation of organs and organ systems is well-developed. The infant is still susceptible to the damaging effects of alcohol.[16]
  • Ethanol exposure in the second trimester reduces nutrition levels and can affect the functioning of the endocrine system in both fetus and mother. This is because blood flow via umbilical artery to fetal brain is reduced.[53][better source needed]


Fetal alcohol spectrum disorders encompass a range of physical and neurodevelopmental problems which can result from prenatal alcohol exposure. Diagnosis is based on the signs and symptoms in the person and evidence of alcohol use.[1] These diagnoses of fetal alcohol spectrum disorders are currently recognized:

  • Fetal alcohol syndrome (FAS)[1]
  • Partial fetal alcohol syndrome (pFAS) refers to individuals with a known, or highly suspected, history of prenatal alcohol exposure who have alcohol-related physical and neurodevelopmental deficits that do not meet the full criteria for FAS.[20]
  • Alcohol-related neurodevelopmental disorder (ARND)[20][1]
  • Neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE)[1]

As of 2016, the Swedish Agency for Health Technology Assessment and Assessment of Social Services accepts only FAS as a diagnosis, seeing the evidence as inconclusive with respect to other types. The agency feels it is unclear if identifying a FASD-related condition benefits the diagnosed individual.[54]


Presently, four FASD diagnostic systems that diagnose FAS and other FASD conditions have been developed in North America:

  • The Institute of Medicine's guidelines for FAS, the first system to standardize diagnoses of individuals with prenatal alcohol exposure;[17]
  • The University of Washington's "The 4-Digit Diagnostic Code", which ranks the four key features of FASD on a Likert scale of one to four and yields 256 descriptive codes that can be categorized into 22 distinct clinical categories, ranging from FAS to no findings;[55]
  • The Centers for Disease Control's "Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis", which established consensus on the diagnosis FAS in the U.S. but deferred addressing other FASD conditions;[56] and
  • Canadian guidelines for FASD diagnoses, which established criteria for diagnosing FASD in Canada and harmonized most differences between the IOM and University of Washington's systems.[2]

Each diagnostic system requires an assessment of four key features: growth, facial features, central nervous system, and alcohol exposure. To determine any FASD condition, a multi-disciplinary evaluation is necessary to assess each of the four key features for assessment. Generally, a trained physician will determine growth deficiency and FAS facial features. While a qualified physician may also assess central nervous system structural abnormalities and/or neurological problems, usually central nervous system damage is determined through psychological, speech-language, and occupational therapy assessments to ascertain clinically significant impairments in three or more of the Ten Brain Domains.[57] Prenatal alcohol exposure risk may be assessed by a qualified physician, psychologist, social worker, or chemical health counselor. These professionals work together as a team to assess and interpret data of each key feature for assessment and develop an integrative, multi-disciplinary report to diagnose FAS (or other FASD conditions) in an individual.[citation needed]

A positive finding on all four features is required for a diagnosis of FAS, and the four diagnostic systems essentially agree on criteria for fetal alcohol syndrome (FAS). However, there are differences among systems when full criteria for FAS are not met. Prenatal alcohol exposure and central nervous system damage are the critical elements of the spectrum of FASD, and a positive finding in these two features is sufficient for an FASD diagnosis in all FASD systems.[citation needed] But different researchers and systems may use a wide variety of terminology to describe an individual's FASD condition, as the nomenclature is still evolving. Most individuals with deficits resulting from prenatal alcohol exposure do not express all features of FAS and fall into other FASD conditions.[17] The Canadian guidelines recommend the assessment and descriptive approach of the "4-Digit Diagnostic Code" for each key feature of FASD and the terminology of the IOM in diagnostic categories, excepting ARBD.[2]

Fetal alcohol syndrome[edit]

The most severe condition is called Fetal Alcohol Syndrome (FAS),[1] which refers to individuals who have a specific set of birth defects and neurodevelopmental disorders characteristic of the diagnosis.[20] The following criteria must be fully met for an FAS diagnosis:[2][17][55][56]

  1. Prenatal or postnatal height or weight (or both) at or below the 10th percentile[13]
  2. All three FAS facial features present[14]
  3. Clinically significant structural, neurological, or functional impairment of the central nervous system
  4. Confirmed or Unknown prenatal alcohol exposure

FAS is the only expression of FASD that has garnered consensus among experts to become an official ICD-9 and ICD-10 diagnosis.

Partial FAS[edit]

Partial FAS (pFAS) was previously known as atypical FAS in the 1997 edition of the "4-Digit Diagnostic Code". People with pFAS have a confirmed history of prenatal alcohol exposure, but may lack growth deficiency or the complete facial stigmata. Central nervous system damage is present at the same level as FAS. These individuals have the same functional disabilities but "look" less like FAS.[citation needed]

The following criteria must be fully met for a diagnosis of Partial FAS:[2][17][55]

  1. Two or three FAS facial features present[14]
  2. Clinically significant structural, neurological, or functional impairment in three or more of the Ten Brain Domains[57]
  3. Confirmed prenatal alcohol exposure

Growth or height may range from normal to deficient.[13]

Alcohol-related neurodevelopmental disorder[edit]

Alcohol-related neurodevelopmental disorder (ARND) is the specific diagnosis of the non-dysmorphic type of FASD, where a majority of the symptoms are witnessed.[58] The diagnosis was initially suggested by the Institute of Medicine to replace the terms FAE (fetal alcohol effects). It focuses on central nervous system damage, rather than growth deficiency or FAS facial features. The Canadian guidelines also use this diagnosis and the same criteria. While the "4-Digit Diagnostic Code" includes these criteria for three of its diagnostic categories, it refers to this condition as static encephalopathy. The behavioral effects of ARND are not necessarily unique to alcohol however, so use of the term must be within the context of confirmed prenatal alcohol exposure.[12] ARND may be gaining acceptance over the terms FAE and ARBD to describe FASD conditions with central nervous system abnormalities or behavioral or cognitive abnormalities or both due to prenatal alcohol exposure without regard to growth deficiency or FAS facial features.[12][59]

The following criteria must be fully met for a diagnosis of ARND or static encephalopathy:[2][17][55]

  1. Minimal or no FAS facial features present[14]
  2. Clinically significant structural, neurological, or functional impairment in three or more of the Ten Brain Domains[57]
  3. Confirmed prenatal alcohol exposure

Growth or height may range from normal to minimally deficient.[13]

Neurobehavioral disorder associated with prenatal alcohol exposure[edit]

Neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE) is the spectrum-wide term for the psychiatric, behavioral, and neurological symptoms of all FASDs. It was introduced into the DSM-V as a "condition for further study" and as a specified condition under, "other specified neurodevelopmental disorders" as a way to better study the behavioral aspects of all FASD disorders.[58]

Specific criteria[edit]


In terms of FASD, growth deficiency is defined as significantly below average height, weight or both due to prenatal alcohol exposure and can be assessed at any point in the lifespan. Growth measurements must be adjusted for parental height, gestational age (for a premature infant), and other postnatal insults (e.g., poor nutrition), although birth height and weight are the preferred measurements.[55] Deficiencies are documented when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the population.[13] Prenatal or postnatal presentation of growth deficits can occur, but are most often postnatal.[60]

Criteria for FASD are least specific in the Institute of Medicine (IOM) diagnostic system ("low birth weight..., decelerating weight not due to nutrition..., [or] disproportional low weight to height" p. 4 of executive summary),[17] while the CDC use the 10th percentile as a cut-off to determine growth deficiency.[56] The "4-Digit Diagnostic Code" allows for mid-range gradations in growth deficiency (between the 3rd and 10th percentiles) and severe growth deficiency at or below the 3rd percentile.[55] Growth deficiency (at severe, moderate, or mild levels) contributes to diagnoses of FAS and pFAS, but not ARND or static encephalopathy.[citation needed]

The "4-Digit Diagnostic Code" from 2004 ranks growth deficiency as follows:[55]

  • Severe: Height and weight at or below the 3rd percentile.
  • Moderate: Either height or weight at or below the 3rd percentile, but not both.
  • Mild: Either height or weight or both between the 3rd and 10th percentiles.
  • None: Height and weight both above the 10th percentile.

In the initial studies that described FAS, growth deficiency was a requirement for inclusion in the studies; thus, all the original people with FAS had growth deficiency as an artifact of sampling characteristics used to establish criteria for the syndrome.[citation needed] That is, growth deficiency is a key feature of FASD because growth deficiency was a criterion for inclusion in the study that defined FAS. Growth deficiency may be less critical for understanding the disabilities of FASD than the neurobehavioral sequelae to the brain damage.[17] Canadian guidelines updated in 2016 deleted growth as a diagnostic criterion.[61]

Facial features[edit]

Smooth philtrum seen on a six-month-old baby with FAS

Several characteristic craniofacial abnormalities are often visible in individuals with FAS.[62] The presence of FAS facial features indicates brain damage, although brain damage may also exist in their absence. FAS facial features (and most other visible, but non-diagnostic, deformities) are believed to be caused mainly during the 10th to 20th week of gestation.[63]

Refinements in diagnostic criteria since 1975 have yielded three distinctive and diagnostically significant facial features which distinguish FAS from other disorders with partially overlapping characteristics.[64][65] The three FAS facial features are:

  • A smooth philtrum: The divot or groove between the nose and upper lip flattens with increased prenatal alcohol exposure.
  • Thin vermilion: The upper lip thins with increased prenatal alcohol exposure.
  • Small palpebral fissures: Eye width decreases with increased prenatal alcohol exposure.

Measurement of FAS facial features uses criteria developed by the University of Washington. The lip and philtrum are measured by a trained physician with the Lip-Philtrum Guide,[66] a five-point Likert scale with representative photographs of lip and philtrum combinations ranging from normal (ranked 1) to severe (ranked 5). Palpebral fissure length (PFL) is measured in millimeters with either calipers or a clear ruler and then compared to a PFL growth chart, also developed by the University of Washington.[14]

Ranking FAS facial features is complicated because the three separate facial features can be affected independently by prenatal alcohol. A summary of the criteria follows:[55][67]

  • Severe: All three facial features ranked independently as severe (lip ranked at 4 or 5, philtrum ranked at 4 or 5, and PFL two or more standard deviations below average).
  • Moderate: Two facial features ranked as severe and one feature ranked as moderate (lip or philtrum ranked at 3, or PFL between one and two standard deviations below average).
  • Mild: A mild ranking of FAS facial features covers a broad range of facial feature combinations:
    • Two facial features ranked severe and one ranked within normal limits,
    • One facial feature ranked severe and two ranked moderate, or
    • One facial feature ranked severe, one ranked moderate and one ranked within normal limits.
  • None: All three facial features ranked within normal limits.

Central nervous system[edit]

Central nervous system (CNS) damage is the primary feature of any FASD diagnosis. Prenatal alcohol exposure, which is classified as a teratogen, can damage the brain across a continuum of gross to subtle impairments, depending on the amount, timing, and frequency of the exposure as well as genetic predispositions of the fetus and mother.[17][68] While functional abnormalities are the behavioral and cognitive expressions of the FASD disability, CNS damage can be assessed in three areas: structural, neurological, and functional impairments.[citation needed]

All four diagnostic systems allow for assessment of CNS damage in these areas, but criteria vary. The IOM system requires structural or neurological impairment for a diagnosis of FAS, but also allows a "complex pattern" of functional anomalies for diagnosing PFAS and ARND.[17] The "4-Digit Diagnostic Code" and CDC guidelines allow for a positive CNS finding in any of the three areas for any FASD diagnosis, but functional anomalies must measure at two standard deviations or worse in three or more functional domains for a diagnosis of FAS, PFAS, and ARND.[55][56] The "4-Digit Diagnostic Code" also allows for an FASD diagnosis when only two functional domains are measured at two standard deviations or worse.[55] The "4-Digit Diagnostic Code" further elaborates the degree of CNS damage according to four ranks:

  • Definite: Structural impairments or neurological impairments for FAS or static encephalopathy.
  • Probable: Significant dysfunction of two standard deviations or worse in three or more functional domains.
  • Possible: Mild to moderate dysfunction of two standard deviations or worse in one or two functional domains or by judgment of the clinical evaluation team that CNS damage cannot be dismissed.
  • Unlikely: No evidence of CNS damage.

Structural abnormalities of the brain are observable, physical damage to the brain or brain structures caused by prenatal alcohol exposure. Structural impairments may include microcephaly (small head size) of two or more standard deviations below the average, or other abnormalities in brain structure (e.g., agenesis of the corpus callosum, cerebellar hypoplasia).[17]

Microcephaly is determined by comparing head circumference (often called occipitofrontal circumference, or OFC) to appropriate OFC growth charts.[13] Other structural impairments must be observed through medical imaging techniques by a trained physician. Because imaging procedures are expensive and relatively inaccessible to most people, diagnosis of FAS is not frequently made via structural impairments, except for microcephaly.[citation needed]

Evidence of a CNS structural impairment due to prenatal alcohol exposure will result in a diagnosis of FAS, and neurological and functional impairments are highly likely.[2][17][55][56]

During the first trimester of pregnancy, alcohol interferes with the migration and organization of brain cells, which can create structural deformities or deficits within the brain.[69] During the third trimester, damage can be caused to the hippocampus, which plays a role in memory, learning, emotion, and encoding visual and auditory information, all of which can create neurological and functional CNS impairments as well.[70]

As of 2002, there were 25 reports of autopsies on infants known to have FAS. The first was in 1973, on an infant who died shortly after birth.[71] The examination revealed extensive brain damage, including microcephaly, migration anomalies, corpus callosum dysgenesis, and a massive neuroglial, leptomeningeal heterotopia covering the left hemisphere.[72]

In 1977, Clarren described a second infant whose mother was a binge drinker. The infant died ten days after birth. The autopsy showed severe hydrocephalus, abnormal neuronal migration, and a small corpus callosum.[72] FAS has also been linked to brainstem and cerebellar changes, agenesis of the corpus callosum and anterior commissure, neuronal migration errors, absent olfactory bulbs, meningomyelocele, and porencephaly.[72]


When structural impairments are not observable or do not exist, neurological impairments are assessed. In the context of FASD, neurological impairments are caused by prenatal alcohol exposure which causes general neurological damage to the central nervous system (CNS), the peripheral nervous system, or the autonomic nervous system. A determination of a neurological problem must be made by a trained physician, and must not be due to a postnatal insult, such as meningitis, concussion, traumatic brain injury, etc.[citation needed]

All four diagnostic systems show virtual agreement on their criteria for CNS damage at the neurological level, and evidence of a CNS neurological impairment due to prenatal alcohol exposure will result in a diagnosis of FAS or pFAS, and functional impairments are highly likely.[2][17][55][56]

Neurological problems are expressed as either hard signs, or diagnosable disorders, such as epilepsy or other seizure disorders, or soft signs. Soft signs are broader, nonspecific neurological impairments, or symptoms, such as impaired fine motor skills, neurosensory hearing loss, poor gait, clumsiness, and poor eye–hand coordination. Many soft signs have norm-referenced criteria, while others are determined through clinical judgment. "Clinical judgment" is only as good as the clinician, and soft signs should be assessed by either a pediatric neurologist, a pediatric neuropsychologist, or both.[citation needed]


When structural or neurological impairments are not observed, all four diagnostic systems allow CNS damage due to prenatal alcohol exposure to be assessed in terms of functional impairments.[2][17][55][56] Functional impairments are deficits, problems, delays, or abnormalities due to prenatal alcohol exposure (rather than hereditary causes or postnatal insults) in observable and measurable domains related to daily functioning, often referred to as developmental disabilities. There is no consensus on a specific pattern of functional impairments due to prenatal alcohol exposure[17] and only CDC guidelines label developmental delays as such,[56] so criteria (and FASD diagnoses) vary somewhat across diagnostic systems.

The four diagnostic systems list various CNS domains that can qualify for functional impairment that can determine an FASD diagnosis:

Ten brain domains[edit]

A recent[when?] effort to standardize assessment of functional CNS damage has been suggested by an experienced FASD diagnostic team in Minnesota. The proposed framework attempts to harmonize IOM, 4-Digit Diagnostic Code, CDC, and Canadian guidelines for measuring CNS damage vis-à-vis FASD evaluations and diagnosis. The standardized approach is referred to as the Ten Brain Domains and encompasses aspects of all four diagnostic systems' recommendations for assessing CNS damage due to prenatal alcohol exposure. The framework provides clear definitions of brain dysfunction, specifies empirical data needed for accurate diagnosis, and defines intervention considerations that address the complex nature of FASD with the intention to avoid common secondary disabilities.[57]

The proposed Ten Brain Domains include:[57]

The Fetal Alcohol Diagnostic Program (FADP) uses unpublished Minnesota state criteria of performance at 1.5 or more standard deviations on standardized testing in three or more of the Ten Brain Domains to determine CNS damage. However, the Ten Brain Domains are easily incorporated into any of the four diagnostic systems' CNS damage criteria, as the framework only proposes the domains, rather than the cut-off criteria for FASD.[73]

Alcohol exposure[edit]

Prenatal alcohol exposure is determined by interview of the biological mother or other family members knowledgeable of the mother's alcohol use during the pregnancy (if available), prenatal health records (if available), and review of available birth records, court records (if applicable), chemical dependency treatment records (if applicable), chemical biomarkers,[74] or other reliable sources.

Exposure level is assessed as confirmed exposure, unknown exposure, and confirmed absence of exposure by the IOM, CDC and Canadian diagnostic systems. The "4-Digit Diagnostic Code" further distinguishes confirmed exposure as High Risk and Some Risk:[citation needed]

  • Confirmed exposure: The CDC guidelines are silent on using information on amount, frequency, and timing of prenatal alcohol use for diagnostic purposes. The IOM and Canadian guidelines explore this further, acknowledging the importance of significant alcohol exposure from regular or heavy episodic alcohol consumption in determining, but offer no standard for diagnosis. Canadian guidelines discuss this lack of clarity and parenthetically point out that "heavy alcohol use" is defined by the National Institute on Alcohol Abuse and Alcoholism as five or more drinks per episode on five or more days during a 30-day period.[75] "The 4-Digit Diagnostic Code" ranking system distinguishes between levels of prenatal alcohol exposure as high risk and some risk. It operationalizes high risk exposure as a blood alcohol concentration (BAC) greater than 100 mg/dL delivered at least weekly in early pregnancy. This BAC level is typically reached by a 55 kg female drinking six to eight beers in one sitting.[55]
    • High Risk: Confirmed use of alcohol during pregnancy known to be at high blood alcohol levels (100 mg/dL or greater) delivered at least weekly in early pregnancy.
    • Some Risk: Confirmed use of alcohol during pregnancy with use less than High Risk or unknown usage patterns.
  • Unknown Risk: Unknown use of alcohol during pregnancy. For many adopted or adults and children in foster care, records or other reliable sources may not be available for review. Reporting alcohol use during pregnancy can also be stigmatizing to birth mothers, especially if alcohol use is ongoing. Many are reluctant to admit to drinking or to provide an accurate report of the quantity they drank.[56] In these cases, all diagnostic systems use an unknown prenatal alcohol exposure designation. A diagnosis of FAS is still possible with an unknown exposure level if other key features of FASD are present at clinical levels.[citation needed]
  • No Risk: Confirmed absence of prenatal alcohol exposure. Confirmed absence of exposure would apply to planned pregnancies in which no alcohol was used or pregnancies of women who do not use alcohol or report no use during the pregnancy. This designation is relatively rare, as most people presenting for an FASD evaluation are at least suspected to have had a prenatal alcohol exposure due to presence of other key features of FASD.[55][56]


Evidence is insufficient for the use of chemical biomarkers to detect prenatal alcohol exposure.[76] Biomarkers being studied include fatty acid ethyl esters (FAEE) detected in the meconium (first feces of an infant) and hair. FAEE may be present if chronic alcohol exposure occurs during the second and third trimester since this is when the meconium begins to form. Concentrations of FAEE can be influence by medication use, diet, and individual genetic variations in FAEE metabolism however.[74][77]

Differential diagnosis[edit]

The CDC reviewed nine syndromes that have overlapping features with FAS; however, none of these syndromes include all three FAS facial features, and none are the result of prenatal alcohol exposure:[56]

Other disorders that have overlapping behavioral symptoms and/or that might be comorbid to fetal alcohol spectrum disorder might include:[78]

Most people with an FASD have most often been misdiagnosed with ADHD due to the large overlap between their behavioral deficits.


A label on alcoholic drinks promoting zero alcohol during pregnancy

Almost all experts recommend that the mother abstain from alcohol use during pregnancy to prevent FASDs.[4][12][79] As the woman may not become aware that she has conceived until several weeks into the pregnancy, it is also recommended to abstain while attempting to become pregnant.[80] These two recommendations have been made by the Surgeon General of the United States,[81][80] the Centers for Disease Control,[21] the American College of Obstetricians and Gynecologists, the American Academy of Pediatrics,[33] the World Health Organization,[82] the United Kingdom's National Institute for Health and Clinical Excellence,[83] and many others.[29][84][31][85][86][87][excessive citations] In the United States, federal legislation has required that warning labels be placed on all alcoholic beverage containers since 1988 under the Alcoholic Beverage Labeling Act.[88]

Women can experience serious symptoms that accompany alcohol withdrawal during pregnancy. According to the World Health Organization, these symptoms can be treated during pregnancy with brief use of benzodiazepine tranquilizers.[19] Currently, the FDA has approved three medications—naltrexone, acamprosate, and disulfiram—for the treatment of alcohol use disorder (AUD). However, there is insufficient data regarding the safety of these medications for pregnant women.[89]

  • Naltrexone is a nonselective opioid antagonist that is used to treat AUD and opioid use disorder.[90] The long-term effects of naltrexone on the fetus are currently unknown.[91] Animal studies show that naltrexone administered during pregnancy increases the incidence of early fetal loss; however, there are insufficient data available to identify the extent to which this is a risk in pregnant women.[92]
  • Acamprosate functions as both an antagonist of NMDA and glutamate and an agonist at GABAA receptors, although its molecular mechanism is not completely understood. Acamprosate has been shown to be effective at preventing alcohol relapse during abstinence.[90] Animal data, however, suggests that acamprosate can have possible teratogenic effects on fetuses.[89]
  • Disulfiram prevents relapse by blocking the metabolism of acetaldehyde after consumption of alcohol which leads to headache, nausea, and vomiting.[90] Some evidence suggests that disulfiram use during the first trimester is associated with an increased risk of congenital malformations such as reduction defects and cleft palate.[91] Additionally, the effects of disulfiram can involve hypertension which can be harmful to both the pregnant woman and the fetus.[89]

American Psychiatric Association guidelines recommend that medications not be used to treat alcohol use disorder in pregnant women except in cases of acute alcohol withdrawals or other co-existing conditions.[93] Instead, behavioral interventions are usually preferred as treatments for pregnant women with AUD. Medications should only be used for pregnant women after carefully considering potential risks and harms of the medications versus the benefits of alcohol cessation.[89]


Although the condition has no available cure, treatment can improve outcomes.[1][3] Because CNS damage, symptoms, secondary disabilities, and needs vary widely by individual, there is no one treatment type that works for everyone.[44]

Between 2017 and 2019 researchers made a breakthrough when they discovered a possible cure using neural stem cells (NSCs); they propose that if applied to a newborn, the damage can be reversed and prevent any lasting effects in the future.[94]


Psychoactive drugs are frequently tried as many FASD symptoms are mistaken for or overlap with other disorders, most notably ADHD. Medications are used to specifically treat symptoms of FASDs and not FAS entirely. Some of the medications used are antidepressants, stimulants, neuroleptics and anti-anxiety drugs.[95]

Behavioral interventions[edit]

Early intervention from birth to age 3 has been shown to improve the development of a child born with FASD.[77] Interventions may include parent–child interaction therapy, efforts to modify child behavior, and drugs.[5] Behavioral interventions are based on the learning theory, which is the basis for many parenting and professional strategies and interventions.[59] Along with ordinary parenting styles, such strategies are frequently used by default for treating those with FAS, as the diagnoses oppositional defiance disorder (ODD), conduct disorder, reactive attachment disorder (RAD) often overlap with FAS (along with ADHD), and these are sometimes thought to benefit from behavioral interventions. Frequently, a person's poor academic achievement results in special education services, which also utilizes principles of learning theory, behavior modification, and outcome-based education.[citation needed]

Children with FAS benefit from behavioral and functional training, social skill training and tutoring. Support groups and talk therapy not only help the children suffering from FAS, but also help the parents and siblings of these children.[citation needed]

Developmental framework[edit]

Many books and handouts on FAS recommend a developmental approach, based on developmental psychology, even though most do not specify it as such and provide little theoretical background. Optimal human development generally occurs in identifiable stages (e.g., Jean Piaget's theory of cognitive development, Erik Erikson's stages of psychosocial development, John Bowlby's attachment framework, and other developmental stage theories). FAS interferes with normal development,[96] which may cause stages to be delayed, skipped, or immaturely developed. Over time, an unaffected child can negotiate the increasing demands of life by progressing through stages of development normally, but not so for a child with FAS.[96]

By knowing what developmental stages and tasks children follow, treatment and interventions for FAS can be tailored to helping a person meet developmental tasks and demands successfully.[96] If a person is delayed in the adaptive behavior domain, for instance, then interventions would be recommended to target specific delays through additional education and practice (e.g., practiced instruction on tying shoelaces), giving reminders, or making accommodations (e.g., using slip-on shoes) to support the desired functioning level. This approach is an advance over behavioral interventions, because it takes the person's developmental context into account while developing interventions.[citation needed]

Advocacy model[edit]

The advocacy model takes the point of view that someone is needed to actively mediate between the environment and the person with FAS.[12] Advocacy activities are conducted by an advocate (for example, a family member, friend, or case manager) and fall into three basic categories. An advocate for FAS: (1) interprets FAS and the disabilities that arise from it and explains it to the environment in which the person operates, (2) engenders change or accommodation on behalf of the person, and (3) assists the person in developing and reaching attainable goals.[12]

The advocacy model is often recommended, for example, when developing an individualized education program (IEP) for the person's progress at school.[95]

An understanding of the developmental framework would presumably inform and enhance the advocacy model, but advocacy also implies interventions at a systems level as well, such as educating schools, social workers, and so forth on best practices for FAS. However, several organizations devoted to FAS also use the advocacy model at a community practice level as well.[97]

Treating FAS at the public health and public policy level promotes FAS prevention and diversion of public resources to assist those with FAS.[12] It is related to the advocacy model but promoted at a systems level (rather than with the individual or family), such as developing community education and supports, state or province level prevention efforts (e.g., screening for maternal alcohol use during OB/GYN or prenatal medical care visits), or national awareness programs. Several organizations and state agencies in the U.S. are dedicated to this type of intervention.[97]


The prognosis of FASD is variable depending on the type, severity, and if treatment is issued.[citation needed] Prognostic disabilities are divided into primary and secondary disabilities.

Primary disabilities[edit]

The primary disabilities of FAS are the functional difficulties with which the child is born as a result of CNS damage due to prenatal alcohol exposure.[98]

Often, primary disabilities are mistaken as behavior problems, but the underlying CNS damage is the originating source of a functional difficulty,[99] rather than a mental health condition, which is considered a secondary disability. The exact mechanisms for functional problems of primary disabilities are not always fully understood, but animal studies have begun to shed light on some correlates between functional problems and brain structures damaged by prenatal alcohol exposure.[12] Representative examples include:

Functional difficulties may result from CNS damage in more than one domain, but common functional difficulties by domain include:[12][59][96][99] Note that this is not an exhaustive list of difficulties.

Secondary disabilities[edit]

The secondary disabilities of FAS are those that arise later in life secondary to CNS damage. These disabilities often emerge over time due to a mismatch between the primary disabilities and environmental expectations; secondary disabilities can be ameliorated with early interventions and appropriate supportive services.[98]

Six main secondary disabilities were identified in a University of Washington research study of 473 subjects diagnosed with FAS, PFAS (partial fetal alcohol syndrome), and ARND (alcohol-related neurodevelopmental disorder):[12][98]

  • Mental health problems: Diagnosed with ADHD, clinical depression, or other mental illness, experienced by over 90% of the subjects
  • Disrupted school experience: Suspended or expelled from school or dropped out of school, experienced by 60% of the subjects (age 12 and older)
  • Trouble with the law: Charged with or convicted of a crime, experienced by 60% of the subjects (age 12 and older)
  • Confinement: For inpatient psychiatric care, inpatient chemical dependency care, or incarcerated for a crime, experienced by about 50% of the subjects (age 12 and older)
  • Inappropriate sexual behavior: Sexual advances, sexual touching, or promiscuity, experienced by about 50% of the subjects (age 12 and older)
  • Alcohol and drug problems: Abuse or dependency, experienced by 35% of the subjects (age 12 and older)

Two additional secondary disabilities exist for adults:[12][98]

  • Dependent living: Group home, living with family or friends, or some sort of assisted living, experienced by 80% of the subjects (age 21 and older)
  • Problems with employment: Required ongoing job training or coaching, could not keep a job, unemployed, experienced by 80% of the subjects (age 21 and older)

Protective factors and strengths[edit]

Eight factors were identified in the same study as universal protective factors that reduced the incidence rate of the secondary disabilities:[12][98]

  • Living in a stable and nurturing home for over 73% of life
  • Being diagnosed with FAS before age six
  • Never having experienced violence
  • Remaining in each living situation for at least 2.8 years
  • Experiencing a "good quality home" (meeting 10 or more defined qualities) from age 8 to 12 years old
  • Having been found eligible for developmental disability (DD) services
  • Having basic needs met for at least 13% of life
  • Having a diagnosis of FAS (rather than another FASD condition)

Malbin (2002) has identified the following areas of interests and talents as strengths that often stand out for those with FASD and should be utilized, like any strength, in treatment planning:[59]

  • Music, playing instruments, composing, singing, art, spelling, reading, computers, mechanics, woodworking, skilled vocations (welding, electrician, etc.), writing, poetry
  • Participation in non-impact sport or physical fitness activities


One study found that the people with FAS had a significantly shorter life expectancy.[6] With the average life span of 34 years old, a study found that 44% of the deaths were of "external cause", with 15% of deaths being suicides.


Globally, one in 10 women drink alcohol during pregnancy. Out of this population, 20% binge drink and have four or more alcoholic drinks per single occasion.[34] The use of alcohol during pregnancy occurs at different rates across the world, potentially due to various cultural differences and legislation. The five countries with the highest prevalence of alcohol use during pregnancy are Ireland (60%), Belarus (47%), Denmark (46%), the UK (41%), and the Russian Federation (37%).[27]

In a recent count, the prevalence of having any FASD disorder was 1 person out of 20, but some people estimate it could be as high as 1 in 7.[7] The rates of FAS and FASD are likely to be underestimated, because of the difficulty in making the diagnosis and the reluctance of clinicians to label children and mothers.[103]


FASD among Australian youth is more common in indigenous Australians.[104] The only states that have registered birth defects in Australian youth are Western Australia, New South Wales, Victoria and South Australia.[105] In Australia, only 12% of Australian health professionals are aware of the diagnostics and symptoms of FASD.[104] In Western Australia, the rate of births resulting in FASD is 0.02 per 1,000 births for non-Indigenous Australians, however among indigenous births the rate is 2.76 per 1,000 births.[105] In Victoria, there have been no registered FASD related births for indigenous Australians, but the rate for the general population in Victoria is 0.01–0.03 per 1000 births.[105] There have been no dedicated FASD clinics within Western Australia, but there are also no nationally supported diagnostic criteria anywhere in Australia.[106] Passive surveillance is a prevention technique used within Australia to assist in monitoring and establishing detectable defects during pregnancy and childhood.[105]


A 2015 review article estimated the overall costs to Canada from FASD at $9.7 billion (including from crime, healthcare, education, etc.).[107]

South Africa[edit]

In South Africa, some populations have rates as high as 9%.[10]

United States[edit]

In the United States, alcohol use at some point during pregnancy is common and appears to be rising in prevalence.[108][109][110][29] In 2006-2010, an estimated 7.6% of pregnant women used alcohol, while 1.4% of pregnant women reported binge drinking during their pregnancy. The highest prevalence estimates of reported alcohol use during pregnancy were among women who are aged 35–44 years (14.3%), white (8.3%), college graduates (10.0%), or employed (9.6%).[111] In 2015, about 10% of pregnant women drank alcohol in the past month, and 20% to 30% drank at some point during the pregnancy.[30] Of pregnant American women, 3.6% met criteria for an alcohol use disorder in a 2001 epidemiological study.[39] As of 2016, the US Centers for Disease Control estimated 3 million women in the United States are at risk of having a baby with FASD.[112]

FASD is estimated to affect between 1-2% and 5% of people in the United States and Western Europe.[113] FAS is believed to occur in between 0.2 and 9 per 1,000 live births in the United States.[113] Using medical and other records, CDC studies have identified 0.2 to 1.5 infants with FAS for every 1,000 live births in certain areas of the United States.[114] A more recent CDC study of 2010 data analyzed medical and other records and found FAS in 0.3 out of 1,000 children from 7 to 9 years of age.[115]

The lifetime cost per child with FAS in the United States was estimated at $2 million (for an overall cost across the country of over $4 billion) by the CDC in 2002.[113]


Before designation[edit]

Some hold that ancient sources describe the negative effects of alcohol during pregnancy,[10] identifying admonitions from ancient Greek, Roman, the Talmud, and the Bible.[116] For example, Plato writes in his fourth-century B.C. Laws (6.775): "Drinking to excess is a practice that is nowhere seemly ... nor yet safe. ... It behooves both bride and bridegroom to be sober ... in order to ensure, as far as possible, in every case that the child that is begotten may be sprung from the loins of sober parents." The sixth-century AD Talmud (Kethuboth 60b) cautions, "One who drinks intoxicating liquor will have ungainly children." However, ancient sources rarely if ever distinguish maternal alcohol consumption from paternal, and are more concerned with conception than pregnancy. The sources can often be viewed as expressing heredity, that children are likely to turn out like their (alcoholic) parents, rather than presenting the modern viewpoint that alcohol itself has an impact.[117][71]

Beer Street and Gin Lane, William Hogarth (1751)

In 1725, in the midst of the Gin Craze, British physicians petitioned the House of Commons on the effects of strong drink when consumed by pregnant women saying that such drinking is "too often the cause of weak, feeble, and distempered children, who must be, instead of an advantage and strength, a charge to their country".[118] There are many other such historical references during that period.[119] Gin specifically was implicated as affecting children's health and causing stillbirth and infant mortality, as depicted in William Hogarth's Gin Lane. In contrast, Hogarth's Beer Street shows commerce and happiness, suggesting that the alcohol in beer was not known to have deleterious effects at this time.[117]

In Gaelic Scotland, according to Martin Martin, the mother and nurse were not allowed to consume ale during pregnancy and breastfeeding.[citation needed]

In the 19th century, Benjamin Rush and Thomas Trotter lobbied against alcohol consumption during pregnancy to avoid dependence and mental deficiency in children.[117] The teetotalism and temperance movements popularized these and other claims,[120][121] including the teratogenic effects of alcohol on animal embryos,[117] but they were often sensationalized, so much so that any finding that alcohol was harmful was largely denounced as propaganda.[119] A prominent observation of possible links between maternal alcohol use and fetal damage was made in 1899 by Dr. William Sullivan, a Liverpool prison physician who noted higher rates of stillbirth for 120 alcoholic female prisoners than their sober female relatives. He suggested the causal agent to be alcohol use.[122] This contradicted the predominating belief at the time that heredity caused intellectual disability, poverty, and criminal behavior, which contemporary studies on the subjects usually concluded.[12] A case study by Henry H. Goddard of the Kallikak family—popular in the early 1900s—represents this earlier perspective,[123] though later researchers have suggested that the Kallikaks almost certainly had FAS.[124] General studies and discussions on alcoholism throughout the mid-1900s were typically based on a heredity argument.[125] Researchers were often temperance advocates and funded by like-minded organizations such as the Anti-Saloon League, so clinicians viewed all such research with heavy skepticism. The temperance movement effectively shut down serious research into the subject for nearly 50 years after Prohibition.[117]

From the 1960s to the 1980s, alcohol was commonly used as a tocolytic, a method to stop preterm labor (born at less than 37 weeks gestation). The method originated with Dr. Fritz Fuchs, the chairman of the department of obstetrics and gynecology at Cornell University Medical College.[126][127] Doctors recommended a small amount of alcohol to calm the uterus during contractions in early pregnancy or Braxton Hicks contractions. In later stages of pregnancy, the alcohol was administered intravenously and often in large amounts. "Women experienced similar effects as occur with oral ingestion, including intoxication, nausea and vomiting, and potential alcohol poisoning, followed by hangovers when the alcohol was discontinued."[128] Vomiting put the mother at a high risk for aspiration and was "a brutal procedure for all involved".[126] Because the alcohol was being given intravenously, the doctor could continue giving the treatment to the mother long after she had passed out, resulting in her being more intoxicated than would otherwise be possible. Such heavy intoxication was highly likely to contribute to FASD.[126] In a 2015 review, ethanol was found to be no better than placebo (sugar water) in suppressing preterm birth and neonatal mortality. Not only was ethanol worse than other beta-mimetic drugs (tocolytic agents) at postponing birth, it also led to a higher rate of low birthweight babies, babies with breathing problems at birth, and neonatal death.[129]

Recognition as a syndrome[edit]

In France in 1957, Jacqueline Rouquette had described 100 children whose parents were alcoholics in a thesis, which was not published. "She gave a good description in certain cases of the facies" according to her mentor, Paul Lemoine.[130] In 1968, Paul Lemoine of Nantes, himself published a study in a French medical journal about children with distinctive features whose mothers were alcoholics.[131]

Independently, in the U.S., Christy Ulleland at University of Washington Medical School conducted an 18-month study in 1968–1969 documenting the risk of maternal alcohol consumption among the offspring of 11 alcoholic mothers.[132] This study is arguably is the true source of the modern understanding.[119] The infants were studied by dysmorphologists Kenneth Lyons Jones and David Weyhe Smith, colleagues of Ulleland at University of Washington,[119] who identified a pattern of "craniofacial, limb, and cardiovascular defects associated with prenatal onset growth deficiency and developmental delay" in eight children. The pattern of malformations indicated that the damage was prenatal. They named these defects "fetal alcohol syndrome".[133] News of the discovery shocked some, while others were skeptical of the findings.[134] While many syndromes are eponymous, i.e. named after the physician first reporting the association of symptoms, Smith named FAS after the causal agent of the symptoms.[135] He reasoned that doing so would encourage prevention, believing that if people knew maternal alcohol consumption caused the syndrome, then abstinence during pregnancy would follow from patient education and public awareness.[135] At the time, nobody was aware of the full range of possible birth defects from FAS or its rate of prevalence.[135]

In 1978, within nine years of the Washington discovery, animal studies, including non-human monkey studies carried out at the University of Washington Primate Center by Sterling Clarren, had confirmed that alcohol was a teratogen. By 1978, 245 cases of FAS had been reported by medical researchers, and the syndrome began to be described as the most frequent known cause of intellectual disability.[citation needed] In 1979, the Washington and Nantes findings were confirmed by a research group in Gothenburg, Sweden.[136] Researchers in France, Sweden, and the United States were struck by how similar these children looked, though they were not related, and how they behaved in the same unfocused and hyperactive manner.[136]

As a spectrum[edit]

Over time, subsequent research and clinical experience suggested that a range of effects could arise from prenatal alcohol exposure. The term fetal alcohol effects (FAE) was used for alcohol-related neurodevelopmental disorder and alcohol-related birth defects.[1] It was initially used in research studies to describe humans and animals in whom teratogenic effects were seen after confirmed prenatal alcohol exposure (or unknown exposure for humans), but without obvious physical anomalies.[137] Smith (1981) described FAE as an "extremely important concept" to highlight the debilitating effects of brain damage, regardless of the growth or facial features.[138] This term fell out of favor with clinicians in the 1990s because it was often regarded by the public as a less severe disability than FAS, when in fact its effects could be just as detrimental.[139] In 1996 the replacement terms ARBD and ARND were introduced. In 2002, the US Congress mandated that the CDC develop diagnostic guidelines for FAS and in 2004 a definition of a term that already had been used by some in the nineties, the Fetal Alcohol Spectrum Disorder (FASD) was adopted,[140]> to include FAS as well as other conditions resulting from prenatal alcohol exposure.[135] Currently, FAS[17][137][133] is the only expression of prenatal alcohol exposure defined by the International Statistical Classification of Diseases and Related Health Problems and assigned ICD-9 and diagnoses.[citation needed]

Alcohol-related birth defects (ARBD), formerly known as possible fetal alcohol effect (PFAE),[137] was a term proposed as an alternative to FAE and PFAE.[141] The IOM presents ARBD as a list of congenital anomalies that are linked to maternal alcohol use but have no key features of FASD.[17] PFAE and ARBD have fallen out of favor because these anomalies are not necessarily specific to maternal alcohol consumption and are not criteria for diagnosis of FASD.[12]

In 2013, the American Psychiatric Association introduced neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE).[58]

Society and culture[edit]


Criminalization of substance use during pregnancy because of harm to the fetus or child is fiercely debated.[142][143] Elizabeth Armstrong has questioned the zero-tolerance approach taken towards alcohol consumption during pregnancy, describing it as a moral panic.[144][145] While heavy alcohol consumption during pregnancy is known to be damaging to the unborn child, the effects of low intakes remain debatable, particularly in the absence of randomized controlled trials (c.f. § Causes).[42][41] The UK's abstinence recommendation was not chosen based on scientific evidence, but rather because it was simple advice that would ensure no one underestimated the risk.[146] Tennessee's 2014 fetal assault law (which expired in 2016) was criticized for not addressing alcohol use.[147][148] The law criminalized opioid use during pregnancy and resulted in women avoiding professional medical care for fear of prosecution.[149] A wide variety of professional organizations oppose criminalization.[150][151] Minnesota, North Dakota, Oklahoma, South Dakota, and Wisconsin have statutory authorization for the involuntary civil commitment of women who abuse alcohol during pregnancy.[152]

2016 CDC controversy[edit]

In 2016, a CDC press release and infographic entitled "More than 3 million US women at risk for alcohol-exposed pregnancy" caused controversy.[153] The CDC release contained the message "The risk is real. Why take the chance?".[154][155] Darlena Cunha of Times Magazine interpreted the infographic as telling all women of child bearing age not to drink at all, in case they might accidentally fall pregnant, and called them "scare tactics" and "shaming recommendations".[156] Julie Beck said that the infographic insinuated that "your womb is a Schrodinger's box and you shouldn't pour alcohol into it unless you've peeked in there to be 100 percent sure the coast is clear".[157] The CDC later clarified that the infographic was not intended to make any new guidelines or recommendations for women who are pre-pregnant, but rather to encourage conversations about alcohol with health professionals.[158] Nonetheless, half of the pregnancies in developed countries and over 80% in developing countries are unplanned. Many women don't realize they are pregnant during the early stages and continue drinking when pregnant.[34]

In fiction[edit]

In Aldous Huxley's 1932 novel Brave New World (where all fetuses are gestated in vitro in a factory), lower caste fetuses are created by receiving alcohol transfusions (Bokanovsky Process) to reduce intelligence and height, thus conditioning them for simple, menial tasks. Connections between alcohol and incubating embryos are made multiple times in the novel.[159]

The main character of the 2009 film Defendor is implied to have the condition.[citation needed]

Tony Loneman, a character in Tommy Orange's 2018 novel There There, was born with fetal alcohol syndrome, which he calls "the Drome".

See also[edit]


  1. ^ ICD-codes in Popova study: R62.8††, R62.8¶¶, P05.9, P07.1, R62.8§§, R62.8‡‡, Q02
  2. ^ Q10.3†, Q38.0*, Q38.0†
  3. ^ R94.1
  4. ^ F91
  5. ^ F80, F80.1, F80.2, F80.9
  6. ^ H65.2,H90.2,H90.5,H65.0
  7. ^ H54,H52.2,H52.6,H54.2/54.4/54.5
  8. ^ F89
  9. ^ P07.3
  10. ^ F10.2/F19.2
  11. ^ Coccygeal fovea (Q14.1‡). Retinal tortuosity (Q14.1§)
  12. ^ Q76.4
  13. ^ F90.0
  14. ^ Q10.0¶
  15. ^ Q75.2


  1. ^ a b c d e f g h i j k l m n o p q "Facts about FASDs". 16 April 2015. Archived from the original on 23 May 2015. Retrieved 10 June 2015.
  2. ^ a b c d e f g h i Chudley AE, Conry J, Cook JL, Loock C, Rosales T, LeBlanc N (March 2005). "Fetal alcohol spectrum disorder: Canadian guidelines for diagnosis". CMAJ. 172 (5 Suppl): S1–S21. doi:10.1503/cmaj.1040302. PMC 557121. PMID 15738468.
  3. ^ a b Rasmussen C, Andrew G, Zwaigenbaum L, Tough S (March 2008). "Neurobehavioural outcomes of children with fetal alcohol spectrum disorders: A Canadian perspective". Paediatrics & Child Health. 13 (3): 185–191. PMC 2529423. PMID 19252695.
  4. ^ a b "Alcohol Use in Pregnancy". 17 April 2014. Archived from the original on 28 June 2015. Retrieved 10 June 2015.
  5. ^ a b Roszel EL (April 2015). "Central nervous system deficits in fetal alcohol spectrum disorder". The Nurse Practitioner. 40 (4): 24–33. doi:10.1097/01.NPR.0000444650.10142.4f. PMID 25774812.
  6. ^ a b Thanh NX, Jonsson E (2016). "Life Expectancy of People with Fetal Alcohol Syndrome". Journal of Population Therapeutics and Clinical Pharmacology. 23 (1): e53–e59. PMID 26962962.
  7. ^ a b May PA, Chambers CD, Kalberg WO, Zellner J, Feldman H, Buckley D, et al. (February 2018). "Prevalence of Fetal Alcohol Spectrum Disorders in 4 US Communities". JAMA. 319 (5): 474–482. doi:10.1001/jama.2017.21896. PMC 5839298. PMID 29411031.
  8. ^ Oh SS, Kim YJ, Jang SI, Park S, Nam CM, Park EC (November 2020). "Hospitalizations and mortality among patients with fetal alcohol spectrum disorders: a prospective study". Scientific Reports. 10 (1): 19512. Bibcode:2020NatSR..1019512O. doi:10.1038/s41598-020-76406-6. PMC 7658994. PMID 33177533.
  9. ^ Hagan JF, Balachova T, Bertrand J, Chasnoff I, Dang E, Fernandez-Baca D, et al. (October 2016). "Neurobehavioral Disorder Associated With Prenatal Alcohol Exposure". Pediatrics. 138 (4). AAP Publications: e20151553. doi:10.1542/peds.2015-1553. PMC 5477054. PMID 27677572.
  10. ^ a b c Riley EP, Infante MA, Warren KR (June 2011). "Fetal alcohol spectrum disorders: an overview". Neuropsychology Review. 21 (2): 73–80. doi:10.1007/s11065-011-9166-x. PMC 3779274. PMID 21499711.
  11. ^ "FASD Fact #1: FASD = Fetal Alcohol Spectrum Disorder". Families Affected by Fetal Alcohol Spectrum Disorder FAFASD. Retrieved 4 December 2020.
  12. ^ a b c d e f g h i j k l m n Streissguth, A. (1997). Fetal Alcohol Syndrome: A Guide for Families and Communities. Baltimore: Brookes Publishing. ISBN 1-55766-283-5.
  13. ^ a b c d e f Clinical growth charts. Archived 3 December 2010 at the Wayback Machine National Center for Growth Statistics. Retrieved on 2007-04-10
  14. ^ a b c d e FAS facial features Archived 27 October 2007 at the Wayback Machine. FAS Diagnostic and Prevention Network, University of Washington. Retrieved on 2007-04-10
  15. ^ Popova S, Lange S, Shield K, Mihic A, Chudley AE, Mukherjee RA, Bekmuradov D, Rehm J (5 March 2016). "Comorbidity of fetal alcohol spectrum disorder: a systematic review and meta-analysis". The Lancet. 387 (10022): 978–987. doi:10.1016/S0140-6736(15)01345-8. ISSN 0140-6736. PMID 26777270. S2CID 24660949.
  16. ^ a b c d e f "An Alcohol-free pregnancy is the best choice for your baby" (PDF). Centers for Disease Control and Prevention. Retrieved 10 August 2017.Public Domain This article incorporates text from this source, which is in the public domain.
  17. ^ a b c d e f g h i j k l m n o p q r s Institute of Medicine Committee to Study Fetal Alcohol Syndrome (1995). Stratton K, Howe C, Battaglia FC (eds.). Fetal alcohol syndrome: diagnosis, epidemiology, prevention, and treatment. Washington, D.C.: National Academy Press. ISBN 978-0-309-05292-4. Archived from the original on 11 March 2016.
  18. ^ Coriale G, Fiorentino D, Di Lauro F, Marchitelli R, Scalese B, Fiore M, Maviglia M, Ceccanti M (2013). "Fetal Alcohol Spectrum Disorder (FASD): neurobehavioral profile, indications for diagnosis and treatment". Rivista di Psichiatria. 48 (5): 359–369. doi:10.1708/1356.15062. PMID 24326748. S2CID 14826585.
  19. ^ a b c "Guidelines for the identification and management of substance use and substance use disorders in pregnancy" (PDF). World Health Organization. 2014. Retrieved 11 August 2017.
  20. ^ a b c d Kingdon D, Cardoso C, McGrath JJ (February 2016). "Research Review: Executive function deficits in fetal alcohol spectrum disorders and attention-deficit/hyperactivity disorder - a meta-analysis". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 57 (2): 116–131. doi:10.1111/jcpp.12451. PMC 5760222. PMID 26251262.
  21. ^ a b c CDC (24 May 2021). "Alcohol Use in Pregnancy". Centers for Disease Control and Prevention. Retrieved 13 September 2021.
  22. ^ Strömland K, Pinazo-Durán MD (2002). "Ophthalmic involvement in the fetal alcohol syndrome: clinical and animal model studies". Alcohol and Alcoholism. 37 (1): 2–8. doi:10.1093/alcalc/37.1.2. PMID 11825849.
  23. ^ Yin X, Li J, Li Y, Zou S (November 2019). "Maternal alcohol consumption and oral clefts: a meta-analysis". British Journal of Oral and Maxillofacial Surgery. 57 (9): 839–846. doi:10.1016/j.bjoms.2019.08.013. PMID 31473040. S2CID 201716448.
  24. ^ "Dangers of Drinking While Pregnant - DrugAbuse.com". drugabuse.com. 27 July 2016. Retrieved 17 November 2018.
  25. ^ Cook JC, Lynch ME, Coles CD (5 June 2019). "Association Analysis: Fetal Alcohol Spectrum Disorder and Hypertension Status in Children and Adolescents". Alcoholism: Clinical and Experimental Research. 43 (8): 1727–1733. doi:10.1111/acer.14121. PMID 31166027. S2CID 174811433. Retrieved 30 March 2023.
  26. ^ "Understanding Fetal Alcohol Spectrum Disorders". National Institute on Alcohol Abuse and Alcoholism (NIAAA). Retrieved 18 March 2024.
  27. ^ a b Popova S, Lange S, Probst C, Gmel G, Rehm J (March 2017). "Estimation of national, regional, and global prevalence of alcohol use during pregnancy and fetal alcohol syndrome: a systematic review and meta-analysis". The Lancet. Global Health. 5 (3): e290–e299. doi:10.1016/S2214-109X(17)30021-9. PMID 28089487. S2CID 5002534.
  28. ^ a b c d Yaffe SJ (2011). Drugs in pregnancy and lactation: a reference guide to fetal and neonatal risk (9 ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 527. ISBN 978-1-60831-708-0. Archived from the original on 10 September 2017.
  29. ^ a b c d Chang. "UpToDate: Alcohol intake and pregnancy". www.uptodate.com. Retrieved 11 September 2021.
  30. ^ a b c "Fetal Alcohol Exposure". April 2015. Archived from the original on 10 June 2015. Retrieved 10 June 2015.
  31. ^ a b "Committee opinion no. 496: At-risk drinking and alcohol dependence: obstetric and gynecologic implications". Obstetrics and Gynecology. 118 (2 Pt 1): 383–388. August 2011. doi:10.1097/AOG.0b013e31822c9906. ISSN 1873-233X. PMID 21775870. S2CID 205474115.
  32. ^ a b Burd L, Blair J, Dropps K (17 May 2012). "Prenatal alcohol exposure, blood alcohol concentrations and alcohol elimination rates for the mother, fetus and newborn". Journal of Perinatology. 32 (9): 652–659. doi:10.1038/jp.2012.57. ISSN 0743-8346. PMID 22595965. S2CID 1513758.
  33. ^ a b Williams JF, Smith VC (2015). "Fetal Alcohol Spectrum Disorders". Pediatrics. 136 (5): e1395–e1406. doi:10.1542/peds.2015-3113. PMID 26482673. S2CID 23752340.
  34. ^ a b c "Counting the costs of drinking alcohol during pregnancy". Bulletin of the World Health Organization. 95 (5): 320–321. 2017. doi:10.2471/BLT.17.030517. PMC 5418824. PMID 28479632. Retrieved 11 August 2017.
  35. ^ Bandoli G, Hayes S, Delker E (2023). "Low to Moderate Prenatal Alcohol Exposure and Neurodevelopmental Outcomes: A Narrative Review and Methodological Considerations". Alcohol Research: Current Reviews. 43 (1): 01. doi:10.35946/arcr.v43.1.01. PMC 10027299. PMID 36950180.
  36. ^ Mamluk L, Edwards HB, Savović J, Leach V, Jones T, Moore TH, et al. (August 2017). "Low alcohol consumption and pregnancy and childhood outcomes: time to change guidelines indicating apparently 'safe' levels of alcohol during pregnancy? A systematic review and meta-analyses". BMJ Open. 7 (7): e015410. doi:10.1136/bmjopen-2016-015410. PMC 5642770. PMID 28775124. S2CID 2941340.
  37. ^ "Pregnancy and alcohol: occasional, light drinking may be safe". Prescrire International. 21 (124): 44–50. February 2012. PMID 22413723.
  38. ^ Welch A (4 February 2016). "CDC to younger women: Better take your birth control before you drink that glass of wine". Los Angeles Times.
  39. ^ a b McHugh RK, Wigderson S, Greenfield SF (June 2014). "Epidemiology of substance use in reproductive-age women". Obstetrics and Gynecology Clinics of North America. 41 (2): 177–189. doi:10.1016/j.ogc.2014.02.001. PMC 4068964. PMID 24845483.
  40. ^ Sundermann AC, Zhao S, Young CL, Lam L, Jones SH, Velez Edwards DR, Hartmann KE (August 2019). "Alcohol Use in Pregnancy and Miscarriage: A Systematic Review and Meta-Analysis". Alcoholism: Clinical and Experimental Research. 43 (8): 1606–1616. doi:10.1111/acer.14124. PMC 6677630. PMID 31194258.
  41. ^ a b Mamluk L, Edwards HB, Savović J, Leach V, Jones T, Moore TH, et al. (August 2017). "Low alcohol consumption and pregnancy and childhood outcomes: time to change guidelines indicating apparently 'safe' levels of alcohol during pregnancy? A systematic review and meta-analyses". BMJ Open. 7 (7): e015410. doi:10.1136/bmjopen-2016-015410. PMC 5642770. PMID 28775124.
  42. ^ a b Flak AL, Su S, Bertrand J, Denny CH, Kesmodel US, Cogswell ME (2014). "The association of mild, moderate, and binge prenatal alcohol exposure and child neuropsychological outcomes: a meta-analysis". Alcoholism: Clinical and Experimental Research. 38 (1): 214–226. doi:10.1111/acer.12214. ISSN 1530-0277. PMID 23905882.
  43. ^ Mamluk L, Jones T, Ijaz S, Edwards HB, Savović J, Leach V, Moore TH, von Hinke S, Lewis SJ, Donovan JL, Lawlor DA, Davey Smith G, Fraser A, Zuccolo L (23 January 2021). "Evidence of detrimental effects of prenatal alcohol exposure on offspring birthweight and neurodevelopment from a systematic review of quasi-experimental studies". International Journal of Epidemiology. 49 (6): 1972–1995. doi:10.1093/ije/dyz272. PMC 7825937. PMID 31993631.
  44. ^ a b Gupta KK, Gupta VK, Shirasaka T (August 2016). "An Update on Fetal Alcohol Syndrome-Pathogenesis, Risks, and Treatment". Alcoholism: Clinical and Experimental Research. 40 (8): 1594–1602. doi:10.1111/acer.13135. PMID 27375266.
  45. ^ Liyanage-Zachariah V, Harding K (2019), Genetic and Epigenetic Perspectives on the Role of Fathers in Fetal Alcohol Spectrum Disorder (PDF), Canada FASD Research Network
  46. ^ Bhuvaneswar CG, Chang G, Epstein LA, Stern TA (2007). "Alcohol Use During Pregnancy: Prevalence and Impact". Primary Care Companion to the Journal of Clinical Psychiatry. 9 (6): 455–460. doi:10.4088/PCC.v09n0608. ISSN 1523-5998. PMC 2139915. PMID 18185825.
  47. ^ Brien JF, Loomis CW, Tranmer J, McGrath M (May 1983). "Disposition of ethanol in human maternal venous blood and amniotic fluid". American Journal of Obstetrics and Gynecology. 146 (2): 181–186. doi:10.1016/0002-9378(83)91050-5. PMID 6846436.
  48. ^ Nava-Ocampo AA, Velázquez-Armenta Y, Brien JF, Koren G (June 2004). "Elimination kinetics of ethanol in pregnant women". Reproductive Toxicology. 18 (4): 613–617. doi:10.1016/j.reprotox.2004.02.012. PMID 15135856.
  49. ^ Warren KR, Li TK (April 2005). "Genetic polymorphisms: impact on the risk of fetal alcohol spectrum disorders". Birth Defects Research. Part A, Clinical and Molecular Teratology. 73 (4): 195–203. doi:10.1002/bdra.20125. PMID 15786496.
  50. ^ Laufer BI, Mantha K, Kleiber ML, Diehl EJ, Addison SM, Singh SM (July 2013). "Long-lasting alterations to DNA methylation and ncRNAs could underlie the effects of fetal alcohol exposure in mice". Disease Models & Mechanisms. 6 (4): 977–992. doi:10.1242/dmm.010975. PMC 3701217. PMID 23580197.
  51. ^ Shabtai Y, Fainsod A (April 2018). "Competition between ethanol clearance and retinoic acid biosynthesis in the induction of fetal alcohol syndrome". Biochemistry and Cell Biology. 96 (2): 148–160. doi:10.1139/bcb-2017-0132. PMID 28982012.
  52. ^ a b "Drinking and Your Pregnancy". pubs.niaaa.nih.gov. Retrieved 16 November 2018.
  53. ^ Bake S, Tingling JD, Miranda RC (5 December 2011). "Ethanol exposure during pregnancy persistently attenuates cranially-directed blood flow in the developing fetus: Evidence from ultrasound imaging in a murine second trimester equivalent model". Alcoholism: Clinical and Experimental Research. 36 (5): 748–758. doi:10.1111/j.1530-0277.2011.01676.x. ISSN 0145-6008. PMC 3297711. PMID 22141380.
  54. ^ "Fetal Alcohol Syndrome (FAS) and Fetal Alcohol Spectrum Disorders (FASD) – conditions and interventions". www.sbu.se. Swedish Agency for Health Technology Assessment and Assessment of Social Services (SBU). 14 December 2016. Archived from the original on 6 June 2017. Retrieved 8 June 2017.
  55. ^ a b c d e f g h i j k l m n o p Astley, S.J. (2004). Diagnostic Guide for Fetal Alcohol Spectrum Disorders: The 4-Digit Diagnostic Code. Seattle: University of Washington. PDF available at FAS Diagnostic and Prevention Network Archived 16 December 2006 at the Wayback Machine. Retrieved on 2007-04-11.
  56. ^ a b c d e f g h i j k l m Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis (PDF). CDC (July 2004). Retrieved on 2019-10-19
  57. ^ a b c d e f Lang J (2006). "Ten Brain Domains: A Proposal for Functional Central Nervous System Parameters for Fetal Alcohol Spectrum Disorder Diagnosis and Follow-up" (PDF). Journal of the FAS Institute. 4: 1–11. Archived from the original (PDF) on 26 September 2006. Retrieved 4 February 2007.
  58. ^ a b c Hagan JF, Balachova T, Bertrand J, Chasnoff I, Dang E, Fernandez-Baca D, et al. (October 2016). "Neurobehavioral Disorder Associated With Prenatal Alcohol Exposure". Pediatrics. 138 (4): e20151553. doi:10.1542/peds.2015-1553. PMC 5477054. PMID 27677572.
  59. ^ a b c d Malbin, D. (2002). Fetal Alcohol Spectrum Disorders: Trying Differently Rather Than Harder. Portland, Oregon: FASCETS, Inc. ISBN 0-9729532-0-5.
  60. ^ Del Campo M, Jones KL (January 2017). "A review of the physical features of the fetal alcohol spectrum disorders". European Journal of Medical Genetics. 60 (1): 55–64. doi:10.1016/j.ejmg.2016.10.004. PMID 27729236. S2CID 33641835.
  61. ^ Cook JL, Green CR, Lilley CM, Anderson SM, Baldwin ME, Chudley AE, et al. (February 2016). "Fetal alcohol spectrum disorder: a guideline for diagnosis across the lifespan". CMAJ. 188 (3): 191–197. doi:10.1503/cmaj.141593. PMC 4754181. PMID 26668194.
  62. ^ Jones KL, Smith DW (August 1975). "The fetal alcohol syndrome". Teratology. 12 (1): 1–10. doi:10.1002/tera.1420120102. PMID 1162620.
  63. ^ Renwick JH, Asker RL (July 1983). "Ethanol-sensitive times for the human conceptus". Early Human Development. 8 (2): 99–111. doi:10.1016/0378-3782(83)90065-8. PMID 6884260.
  64. ^ Astley SJ, Clarren SK (July 1996). "A case definition and photographic screening tool for the facial phenotype of fetal alcohol syndrome". The Journal of Pediatrics. 129 (1): 33–41. doi:10.1016/s0022-3476(96)70187-7. PMID 8757560.
  65. ^ Astley SJ, Stachowiak J, Clarren SK, Clausen C (November 2002). "Application of the fetal alcohol syndrome facial photographic screening tool in a foster care population". The Journal of Pediatrics. 141 (5): 712–717. doi:10.1067/mpd.2002.129030. PMID 12410204.
  66. ^ Lip-philtrum guides Archived 8 February 2007 at the Wayback Machine. FAS Diagnostic and Prevention Network, University of Washington. Retrieved on 2007-04-10.
  67. ^ Astley, Susan. Backside of Lip-Philtrum Guides (2004) (PDF) Archived 19 June 2007 at the Wayback Machine. University of Washington, Fetal Alcohol Syndrome Diagnostic and Prevention Network. Retrieved on 2007-04-11
  68. ^ West, J.R. (Ed.) (1986). Alcohol and Brain Development. New York: Oxford University Press.[page needed]
  69. ^ Clarren SK, Alvord EC, Sumi SM, Streissguth AP, Smith DW (January 1978). "Brain malformations related to prenatal exposure to ethanol". The Journal of Pediatrics. 92 (1): 64–67. doi:10.1016/S0022-3476(78)80072-9. PMID 619080.
  70. ^ Coles CD, Brown RT, Smith IE, Platzman KA, Erickson S, Falek A (1991). "Effects of prenatal alcohol exposure at school age. I. Physical and cognitive development". Neurotoxicology and Teratology. 13 (4): 357–367. doi:10.1016/0892-0362(91)90084-A. PMID 1921915.
  71. ^ a b Jones KL, Smith DW (November 1973). "Recognition of the fetal alcohol syndrome in early infancy". Lancet. 302 (7836): 999–1001. doi:10.1016/s0140-6736(73)91092-1. PMID 4127281.
  72. ^ a b c Mattson, S.N., & Riley, E.P. (2002). "Neurobehavioral and Neuroanatomical Effects of Heavy Prenatal Exposure to Alcohol," in Streissguth and Kantor. (2002). p. 10.
  73. ^ "fadpmn.org, Nisan 2022". fadpmn.org. Archived from the original on 23 February 2007.
  74. ^ a b Bager H, Christensen LP, Husby S, Bjerregaard L (February 2017). "Biomarkers for the Detection of Prenatal Alcohol Exposure: A Review". Alcoholism: Clinical and Experimental Research. 41 (2): 251–261. doi:10.1111/acer.13309. PMID 28098942. S2CID 2595225.
  75. ^ U.S. Department of Health and Human Services. (2000). National Institute on Alcohol Abuse and Alcoholism. Tenth special report to the U.S Congress on alcohol and health: Highlights frfom current research. Washington, DC: The Institute.
  76. ^ McQuire C, Paranjothy S, Hurt L, Mann M, Farewell D, Kemp A (September 2016). "Objective Measures of Prenatal Alcohol Exposure: A Systematic Review" (PDF). Pediatrics. 138 (3): e20160517. doi:10.1542/peds.2016-0517. PMID 27577579. S2CID 420106.
  77. ^ a b Dejong K, Olyaei A, Lo JO (March 2019). "Alcohol Use in Pregnancy". Clinical Obstetrics and Gynecology. 62 (1): 142–155. doi:10.1097/GRF.0000000000000414. PMC 7061927. PMID 30575614.
  78. ^ "Alcohol and Pregnancy Questions and Answers | FASD | NCBDDD | CDC". www.cdc.gov. 4 August 2017. Retrieved 25 September 2017.
  79. ^ a b Carmona RH (2005). "A 2005 Message to Women from the U.S. Surgeon General" (PDF). Archived (PDF) from the original on 24 September 2015. Retrieved 12 June 2015.
  80. ^ Rankin L (23 August 2011). Fertility, Pregnancy, and Childbirth. St. Martin's Press. p. 14. ISBN 978-1-4299-5932-2. In 1981, the surgeon general put out the now-ubiquitous warning about alcohol and pregnancy.
  81. ^ "Framework for alcohol policy in the WHO European Region" (PDF). World Health Organisation. Archived from the original (PDF) on 3 May 2010. Retrieved 15 March 2024.
  82. ^ "Drinking alcohol while pregnant". NHS. 2 December 2020. Archived from the original on 31 December 2020. Retrieved 31 December 2020.
  83. ^ Williams JF, Smith VC, COMMITTEE ON SUBSTANCE ABUSE (2015). "Fetal Alcohol Spectrum Disorders". Pediatrics. 136 (5): e1395–1406. doi:10.1542/peds.2015-3113. ISSN 1098-4275. PMID 26482673. S2CID 23752340.
  84. ^ Williams JF, Smith VC, COMMITTEE ON SUBSTANCE ABUSE (November 2015). "Fetal Alcohol Spectrum Disorders". Pediatrics. 136 (5): e1395–1406. doi:10.1542/peds.2015-3113. ISSN 1098-4275. PMID 26482673. S2CID 23752340.
  85. ^ Carson G, Cox LV, Crane J, Croteau P, Graves L, Kluka S, Koren G, Martel MJ, Midmer D, Nulman I, Poole N (August 2010). "Alcohol use and pregnancy consensus clinical guidelines". Journal of Obstetrics and Gynaecology Canada. 32 (8 Suppl 3): S1–31. doi:10.1016/s1701-2163(16)34633-3. ISSN 1701-2163. PMID 21172102.
  86. ^ "Alcohol guidelines". Australian Government National Health and Medical Research Council. Archived from the original on 5 November 2012. Retrieved 4 November 2012.
  87. ^ Deaver EL (1 January 1997). "History and implications of the Alcoholic Beverage Labeling Act of 1988". Journal of Substance Misuse. 2 (4): 234–237. doi:10.3109/14659899709081975. ISSN 1357-5007.
  88. ^ a b c d DeVido J, Bogunovic O, Weiss RD (2015). "Alcohol Use Disorders in Pregnancy". Harvard Review of Psychiatry. 23 (2): 112–121. doi:10.1097/HRP.0000000000000070. ISSN 1067-3229. PMC 4530607. PMID 25747924.
  89. ^ a b c Fairbanks J, Umbreit A, Kolla BP, Karpyak VM, Schneekloth TD, Loukianova LL, Sinha S (1 September 2020). "Evidence-Based Pharmacotherapies for Alcohol Use Disorder: Clinical Pearls". Mayo Clinic Proceedings. 95 (9): 1964–1977. doi:10.1016/j.mayocp.2020.01.030. ISSN 0025-6196. PMID 32446635. S2CID 218872499.
  90. ^ a b Thibaut F, Chagraoui A, Buckley L, Gressier F, Labad J, Lamy S, Potenza MN, Kornstein SG, Rondon M, Riecher-Rössler A, Soyka M (2 January 2019). "WFSBP and IAWMH Guidelines for the treatment of alcohol use disorders in pregnant women". The World Journal of Biological Psychiatry. 20 (1): 17–50. doi:10.1080/15622975.2018.1510185. ISSN 1562-2975. PMID 30632868. S2CID 58586890.
  91. ^ Alkermes. VIVITROL (naltrexone for extended-release injectable suspension) U.S. Food and Drug Administration website. https://www.accessdata.fda.gov/drugsatfda_docs/label/2021/021897s052lbl.pdf. Revised March 2021. Accessed September 12, 2021.
  92. ^ Reus VI, Fochtmann LJ, Bukstein O, Eyler AE, Hilty DM, Horvitz-Lennon M, Mahoney J, Pasic J, Weaver M, Wills CD, McIntyre J (1 January 2018). "The American Psychiatric Association Practice Guideline for the Pharmacological Treatment of Patients With Alcohol Use Disorder". American Journal of Psychiatry. 175 (1): 86–90. doi:10.1176/appi.ajp.2017.1750101. ISSN 0002-953X. PMID 29301420.
  93. ^ Lippert T, Gelineau L, Napoli E, Borlongan CV (January 2018). "Harnessing neural stem cells for treating psychiatric symptoms associated with fetal alcohol spectrum disorder and epilepsy". Progress in Neuro-Psychopharmacology & Biological Psychiatry. 80 (Pt A): 10–22. doi:10.1016/j.pnpbp.2017.03.021. PMID 28365374. S2CID 30200836.
  94. ^ a b Buxton, B. (2005). Damaged Angels: An Adoptive Mother Discovers the Tragic Toll of Alcohol in Pregnancy. New York: Carroll & Graf. ISBN 0-7867-1550-2.
  95. ^ a b c d McCreight, B. (1997). Recognizing and Managing Children with Fetal Alcohol Syndrome/Fetal Alcohol Effects: A Guidebook. Washington, DC: CWLA. ISBN 0-87868-607-X.
  96. ^ a b National Organization on Fetal Alcohol Syndrome, Archived 5 April 2007 at the Wayback Machine Minnesota Organization on Fetal Alcohol Syndrome. Archived 5 April 2007 at the Wayback Machine Retrieved on 2007-04-11
  97. ^ a b c d e Streissguth, A.P., Barr, H.M., Kogan, J., & Bookstein, F.L. (1996). Understanding the occurrence of secondary disabilities in clients with fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE): Final report to the Centers for Disease Control and Prevention on Grant No. RO4/CCR008515 (Tech. Report No. 96-06). Seattle: University of Washington, Fetal Alcohol and Drug Unit.
  98. ^ a b Malbin, D. (1993). Fetal Alcohol Syndrome, Fetal Alcohol Effects: Strategies for Professionals. Center City, MN: Hazelden. ISBN 0-89486-951-5
  99. ^ Abel EL, Jacobson S, Sherwin BT (1983). "In utero alcohol exposure: functional and structural brain damage". Neurobehavioral Toxicology and Teratology. 5 (3): 363–366. PMID 6877477.
  100. ^ Meyer LS, Kotch LE, Riley EP (1990). "Neonatal ethanol exposure: functional alterations associated with cerebellar growth retardation". Neurotoxicology and Teratology. 12 (1): 15–22. doi:10.1016/0892-0362(90)90107-N. PMID 2314357.
  101. ^ Zimmerberg B, Mickus LA (December 1990). "Sex differences in corpus callosum: influence of prenatal alcohol exposure and maternal undernutrition". Brain Research. 537 (1–2): 115–122. doi:10.1016/0006-8993(90)90347-e. PMID 2085766. S2CID 21989095.
  102. ^ Larkby C, Day N (1997). "The effects of prenatal alcohol exposure". Alcohol Health and Research World. 21 (3): 192–198. ISSN 0090-838X. PMC 6826810. PMID 15706768.
  103. ^ a b Elliott EJ, Payne J, Haan E, Bower C (November 2006). "Diagnosis of foetal alcohol syndrome and alcohol use in pregnancy: a survey of paediatricians' knowledge, attitudes and practice". Journal of Paediatrics and Child Health. 42 (11): 698–703. doi:10.1111/j.1440-1754.2006.00954.x. PMID 17044897. S2CID 22479922.
  104. ^ a b c d Burns L, Breen C, Bower C, O' Leary C, Elliott EJ (September 2013). "Counting fetal alcohol spectrum disorder in Australia: the evidence and the challenges". Drug and Alcohol Review. 32 (5): 461–467. doi:10.1111/dar.12047. PMID 23617437.
  105. ^ Mutch RC, Watkins R, Bower C (April 2015). "Fetal alcohol spectrum disorders: notifications to the Western Australian Register of Developmental Anomalies". Journal of Paediatrics and Child Health. 51 (4): 433–436. doi:10.1111/jpc.12746. PMID 25412883. S2CID 25740666.
  106. ^ Thanh NX, Jonsson E (2015). "Costs of Fetal Alcohol Spectrum Disorder in the Canadian Criminal Justice System". Journal of Population Therapeutics and Clinical Pharmacology. 22 (1): e125-31. PMID 26072470. Retrieved 14 November 2022.
  107. ^ Denny CH, Acero CS, Naimi TS, Kim SY (26 April 2019). "Consumption of Alcohol Beverages and Binge Drinking Among Pregnant Women Aged 18-44 Years - United States, 2015-2017". MMWR. Morbidity and Mortality Weekly Report. 68 (16): 365–368. doi:10.15585/mmwr.mm6816a1. ISSN 1545-861X. PMC 6483284. PMID 31022164.
  108. ^ Centers for Disease Control and Prevention (CDC) (20 July 2012). "Alcohol use and binge drinking among women of childbearing age--United States, 2006-2010". MMWR. Morbidity and Mortality Weekly Report. 61 (28): 534–538. ISSN 1545-861X. PMID 22810267.
  109. ^ Tan CH, Denny CH, Cheal NE, Sniezek JE, Kanny D (25 September 2015). "Alcohol use and binge drinking among women of childbearing age - United States, 2011-2013". MMWR. Morbidity and Mortality Weekly Report. 64 (37): 1042–1046. doi:10.15585/mmwr.mm6437a3. ISSN 1545-861X. PMID 26401713.
  110. ^ Centers for Disease Control and Prevention (CDC) (20 July 2012). "Alcohol use and binge drinking among women of childbearing age--United States, 2006-2010". MMWR. Morbidity and Mortality Weekly Report. 61 (28): 534–538. ISSN 1545-861X. PMID 22810267.
  111. ^ "More than 3 million US women at risk for alcohol-exposed pregnancy | CDC Online Newsroom | CDC". www.cdc.gov. 2 February 2016. Archived from the original on 21 November 2016. Retrieved 20 November 2016.
  112. ^ a b c "Data & Statistics Prevalence of FASDs". Center for Disease Control and Prevention. 16 April 2015. Archived from the original on 29 June 2015. Retrieved 10 June 2015.
  113. ^ "Fetal Alcohol Syndrome --- Alaska, Arizona, Colorado, and New York, 1995--1997". www.cdc.gov. Retrieved 13 September 2021.
  114. ^ "Fetal Alcohol Syndrome Among Children Aged 7–9 Years — Arizona, Colorado, and New York, 2010". www.cdc.gov. Retrieved 13 September 2021.
  115. ^ Oba PS (2007). "History of FASD". FAS Aware UK. Archived from the original on 4 January 2017. Retrieved 20 November 2016.
  116. ^ a b c d e Sanders JL (2009). "Were our forebears aware of prenatal alcohol exposure and its effects? A review of the history of fetal alcohol spectrum disorder". The Canadian Journal of Clinical Pharmacology = Journal Canadien de Pharmacologie Clinique. 16 (2): e288-95. PMID 19439773.
  117. ^ Jackson R (24 April 1828). Valpy AJ (ed.). "Considerations on the Increase of Crime, and the Degree of its Extent". The Pamphleteer. 29 (57). London: John Hatchard and Son ... and T. and G. Underwood ...: 325. OCLC 1761801. [Alcohol consumption is] too often the cause of weak, feeble, and distempered children, who must be, instead of an advantage and strength, a charge to their country. Biography of author Randle Jackson
  118. ^ a b c d Price AD (2021). "Overview of FASD: How Our Understanding of FASD Has Progressed". Prevention, Recognition and Management of Fetal Alcohol Spectrum Disorders. pp. 9–22. doi:10.1007/978-3-030-73966-9_2. ISBN 978-3-030-73965-2.
  119. ^ Jonathan Townley Crane, Arts of Intoxication: The Aim and the Results (New York: Carlton & Lanahan, 1870), 173–175
  120. ^ Jennifer L. Tait, The Poisoned Chalice (Tuscaloosa, Alabama: University of Alabama Press, 2010), 27,28.
  121. ^ Sullivan WC (1899). "A note on the influence of maternal inebriety on the offspring". Journal of Mental Science. 45 (190): 489–503. doi:10.1192/bjp.45.190.489.
  122. ^ Goddard, H. H. (1912). The Kallikak Family: A Study in the Heredity of Feeble-Mindedness. New York: Macmillan.
  123. ^ Karp RJ, Qazi QH, Moller KA, Angelo WA, Davis JM (January 1995). "Fetal alcohol syndrome at the turn of the 20th century: An unexpected explanation of the Kallikak family". Archives of Pediatrics & Adolescent Medicine. 149 (1): 45–48. doi:10.1001/archpedi.1995.02170130047010. PMID 7827659.
  124. ^ Haggard, H. W., & Jellinek, E. M. (1942). Alcohol Explored. New York: Doubleday.
  125. ^ a b c Armstrong, E. M. (2003). Conceiving risk, bearing responsibility: Fetal alcohol syndrome & the diagnosis of moral disorder. Baltimore: The Johns Hopkins University Press.
  126. ^ Saxon W (4 March 1995). "Dr. Fritz Fuchs, 76, Who Advanced Obstetrics". The New York Times. Archived from the original on 27 June 2017. Retrieved 16 February 2017.
  127. ^ King, T. L., & Brucker, M. C. (2011). Pharmacology for women's health. Sudbury, MA: Jones and Bartlett.
  128. ^ Haas DM, Morgan AM, Deans SJ, Schubert FP (5 November 2015). "Ethanol for preventing preterm birth in threatened preterm labor". Cochrane Database of Systematic Reviews. 2015 (11): CD011445. doi:10.1002/14651858.CD011445.pub2. PMC 8944412. PMID 26544539.
  129. ^ Lemoine P (August 1994). "The letter from Professor Lemoine". Addiction. 89 (8): 1021–1023. doi:10.1111/j.1360-0443.1994.tb03364.x. ISSN 0965-2140.
  130. ^ Lemoine P., Harousseau H., Borteyru J.B., Menuet J.C. (1968). "Les enfants de parents alcooliques. Anomalies observées, à propos de 127 cas". Quest Medical. 21: 476–482. Reprinted in Lemoine P, Harousseau H, Borteyru JP, Menuet JC (April 2003). "Children of alcoholic parents--observed anomalies: discussion of 127 cases". Therapeutic Drug Monitoring. 25 (2): 132–136. doi:10.1097/00007691-200304000-00002. PMID 12657907. S2CID 8894309.
  131. ^ Ulleland CN (May 1972). "The offspring of alcoholic mothers". Annals of the New York Academy of Sciences. 197 (1): 167–169. Bibcode:1972NYASA.197..167U. doi:10.1111/j.1749-6632.1972.tb28142.x. PMID 4504588. S2CID 84514766.
  132. ^ a b Jones KL, Smith DW, Ulleland CN, Streissguth P (June 1973). "Pattern of malformation in offspring of chronic alcoholic mothers". Lancet. 1 (7815): 1267–1271. doi:10.1016/S0140-6736(73)91291-9. PMID 4126070.
  133. ^ Streissguth, A.P. (2002). In A. Streissguth, & J. Kanter (Eds.), The Challenge in Fetal Alcohol Syndrome: Overcoming Secondary Disabilities. Seattle: University of WA Press. ISBN 0-295-97650-0.
  134. ^ a b c d Clarren, S.K. (2005). A thirty year journey from tragedy to hope. Foreword to Buxton, B. (2005). Damaged Angels: An Adoptive Mother Discovers the Tragic Toll of Alcohol in Pregnancy. New York: Carroll & Graf. ISBN 0-7867-1550-2.
  135. ^ a b Olegård R, Sabel KG, Aronsson M, Sandin B, Johansson PR, Carlsson C, et al. (1979). "Effects on the child of alcohol abuse during pregnancy. Retrospective and prospective studies". Acta Paediatrica Scandinavica. Supplement. 275: 112–121. doi:10.1111/j.1651-2227.1979.tb06170.x. PMID 291283. S2CID 2799171.
  136. ^ a b c Clarren SK, Smith DW (May 1978). "The fetal alcohol syndrome". The New England Journal of Medicine. 298 (19): 1063–1067. doi:10.1056/NEJM197805112981906. PMID 347295.
  137. ^ Smith DW (1981). "Fetal alcohol syndrome and fetal alcohol effects". Neurobehavioral Toxicology and Teratology. 3 (2): 127. PMID 7254460.
  138. ^ Aase JM, Jones KL, Clarren SK (March 1995). "Do we need the term "FAE"?". Pediatrics. 95 (3): 428–430. PMID 7862486.
  139. ^ Williams JF, Smith VC (November 2015). "Fetal Alcohol Spectrum Disorders". Pediatrics. 136 (5): e1395–e1406. doi:10.1542/peds.2015-3113. PMID 26482673. S2CID 23752340.
  140. ^ Sokol RJ, Clarren SK (August 1989). "Guidelines for use of terminology describing the impact of prenatal alcohol on the offspring". Alcoholism: Clinical and Experimental Research. 13 (4): 597–598. doi:10.1111/j.1530-0277.1989.tb00384.x. PMID 2679217.
  141. ^ Angelotta C, Appelbaum PS (June 2017). "Criminal Charges for Child Harm from Substance Use in Pregnancy". The Journal of the American Academy of Psychiatry and the Law. 45 (2): 193–203. PMID 28619859.
  142. ^ Hackler C (November 2011). "Ethical, legal and policy issues in management of fetal alcohol spectrum disorder". The Journal of the Arkansas Medical Society. 108 (6): 123–4. PMC 4049518. PMID 23252025.
  143. ^ Armstrong EM, Abel EL (2000). "Fetal alcohol syndrome: the origins of a moral panic". Alcohol and Alcoholism. 35 (3): 276–282. doi:10.1093/alcalc/35.3.276. ISSN 0735-0414. PMID 10869248.
  144. ^ Armstrong EM (2017). "Making Sense of Advice About Drinking During Pregnancy: Does Evidence Even Matter?". The Journal of Perinatal Education. 26 (2): 65–69. doi:10.1891/1058-1243.26.2.65. PMC 6353268. PMID 30723369.
  145. ^ "'No alcohol in pregnancy' advised". 25 May 2007.
  146. ^ Humphrey T (20 March 2016). "Legislators clash with doctors, judges over renewing fetal assault law". Knoxville News Sentinel.
  147. ^ Bassett L (30 April 2014). "State Enacts Law To Incarcerate Pregnant Women Who Use Drugs". HuffPost.
  148. ^ Darlington CK, Compton PA, Hutson SP (May 2021). "Revisiting the Fetal Assault Law in Tennessee: Implications and the Way Forward". Policy, Politics, & Nursing Practice. 22 (2): 93–104. doi:10.1177/1527154421989994. PMID 33567969.
  149. ^ Picciuto E (9 December 2014). "Court Says Fetal Alcohol Syndrome Isn't a Crime". The Daily Beast.
  150. ^ "Medical and Public Health Groups Oppose Punishment of Pregnant People". Pregnancy Justice. 2023. Retrieved 15 March 2024.
  151. ^ "Civil Commitment: About This Policy". Alcohol Policy Information System. NIAAA. Retrieved 15 March 2024.
  152. ^ "CDC faces backlash over alcohol warning to women". Retrieved 6 April 2018.
  153. ^ "More than 3 million US women at risk for alcohol-exposed pregnancy". Centers for Disease Control and Prevention. 2 February 2016.
  154. ^ "Alcohol and Pregnancy | VitalSigns | CDC". www.cdc.gov. 20 March 2017. Archived from the original on 26 September 2016. Retrieved 6 April 2018.
  155. ^ "The CDC's Alcohol and Pregnancy Warning Shames Women". Time. 5 February 2016. Retrieved 6 April 2018.
  156. ^ Khazan O, Beck J (3 February 2016). "CDC to Women: Don't Drink Unless You're On Birth Control". The Atlantic. Retrieved 15 March 2024.
  157. ^ Schumaker E (4 February 2016). "No, The Government Did Not Just Tell Women To Stop Drinking". HuffPost. Retrieved 15 March 2024.
  158. ^ Brown JM, Bland R, Jonsson E, Greenshaw AJ (March 2019). "A Brief History of Awareness of the Link Between Alcohol and Fetal Alcohol Spectrum Disorder". Canadian Journal of Psychiatry. 64 (3): 164–168. doi:10.1177/0706743718777403. PMC 6405809. PMID 29807454.

External links[edit]