Fetal alcohol spectrum disorder

The key signs of fetal alcohol syndrome (FAS) required for diagnosis include: • Growth deficiency or failure to thrive: slow fetal growth low birth weight or height, small head circumference (microcephaly) • Conduct disorder, behavioral problems, disruptive behavior, or impulsivity • Developmental language disorder • Hearing loss • Visual impairment, including blindness or astigmatism • Developmental delay, cognitive disorder, or mental deficiency • Premature birth • Substance dependence • Congenital malformation of retina • Congenital fusion of cervical vertebrae or cervical spine fusion • Attention deficit hyperactivity disorder (ADHD) or otherwise impaired attention • Small eye openings (blepharophimosis), or an abnormally increased distance between the eyes, or both (hypertelorism) 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. 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. • Intellectual disability, both in overall IQ measurements and in many functional tests • Fetal mortality, such as spontaneous abortion (miscarriage), stillbirth, and sudden infant death syndrome • Heart: A heart murmur that frequently disappears by one year of age. Ventricular septal defect, atrial septal defect, tetralogy of Fallot, coarctation of the aorta, or cardiac rhythm dysfunction. • Bones: Joint anomalies including abnormal position and function, altered palmar crease patterns, small distal phalanges, and small fifth fingernails. • Kidneys: Horseshoe, aplastic, dysplastic, or hypoplastic kidneys. • Eyes: Strabismus, optic nerve hypoplasia (which may cause light sensitivity, decreased visual acuity, or involuntary eye movements). • Cleft lip with or without a cleft palate: Alcohol is known to be a folic acid antagonist, and a baby's palate and lip develop during the first trimester of the pregnancy (first 12 weeks). Heavy alcohol consumption and binge drinking during this time have been linked to orofacial cleft. • Occasional problems: ptosis of the eyelid, microphthalmia, webbed neck, short neck, radioulnar synostosis, spina bifida, and hydrocephalus. 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, does not sleep properly, weakening of sucking ability and increased hunger. In 2019, a study found that individuals with FASD have a higher risk of hypertension independent of race/ethnicity and obesity. ==Causes==

Fetal alcohol spectrum disorders are caused by alcohol exposure during gestational development. However, not all infants exposed to alcohol in utero will have detectable FAS, FASD, or pregnancy complications. Because alcohol is a known teratogen, it is considered unethical to do randomized controlled trials on pregnant women to determine the precise toxicity effects of alcohol. Among women who consume any quantity of alcohol 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 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. Among those mothers who have an alcohol use disorder, an estimated one-third of their children have FAS. The variance seen in outcomes of alcohol consumption during pregnancy is poorly understood. Aggravating factors may include low maternal weight, advanced maternal age, smoking, poor diet, genetics, and social risk factors. Blood alcohol concentration has been identified as a relevant factor. 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". 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. The evidence is inconsistent and contradictory regarding the effects of low-to-moderate drinking, for example, less than 12 grams of ethanol per day. 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 sources. 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. but this has been challenged; evidence it can cause complete FAS is inconclusive. == Prevention and stigma ==

promoting zero alcohol during pregnancy Almost all experts recommend that the mother abstain from alcohol use during pregnancy to prevent FASDs. A pregnant woman may not become aware that she has conceived until several weeks into the pregnancy, so it is also recommended to abstain from alcohol while attempting to become pregnant. the Centers for Disease Control, the United Kingdom's National Institute for Health and Clinical Excellence, and many others. Stigma The most current advocacy perspectives encourage people and systems to approach FASD with interventions and support for individuals already living with FASD. Focusing on prevention often only further stigmatizes individuals with FASD and their birth parents. Advocates say, if a person is supporting people currently living with FASD, then that person is spreading the awareness needed for successful prevention efforts; "Intervention is Prevention". Many social determinants of health impact the effects of PAE: • Genetics • Poverty/Access to nutritious food • Malnutrition • Poor social support networks • Lack of personal autonomy • Access to healthcare • Generational and sociocultural traumas • Access to mental health care and treatment Medication 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. • Naltrexone is a nonselective opioid antagonist that is used to treat AUD and opioid use disorder. The long-term effects of naltrexone on the fetus are currently unknown. 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. • 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 is effective at preventing alcohol relapse during abstinence. Instead, behavioral interventions are usually preferred as treatments for pregnant women with AUD. Medications should only be used for pregnant women after carefully considering the potential risks and harms of the medications versus the benefits of alcohol cessation. ==Mechanism==

After a pregnant woman 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. A human fetus appears to be at triple risk from maternal alcohol consumption: • The placenta allows free entry of ethanol and toxic metabolites like acetaldehyde into the fetal compartment. The so-called placental barrier is practically absent concerning ethanol. • The developing fetal nervous system appears particularly sensitive to ethanol toxicity. The latter interferes with proliferation, differentiation, neuronal migration, axonal outgrowth, integration, and fine-tuning of the synaptic network. In short, all major processes in the developing central nervous system appear compromised. • Fetal tissues are quite different from adult tissues in function and purpose. For example, the main detoxifying 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. 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. 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. Developmental stages 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: • From conception 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 in these systems and organs. • 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. ==Diagnosis==

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. Classification 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; and • Canadian guidelines for FASD diagnoses, which established criteria for diagnosing FASD in Canada and harmonized most differences between the IOM and the University of Washington's systems. 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 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. 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. 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. The following criteria must be fully met for an FAS diagnosis: The following criteria must be fully met for a diagnosis of Partial FAS: The following criteria must be fully met for a diagnosis of ARND or static encephalopathy: Specific criteria Growth 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. Prenatal or postnatal presentation of growth deficits can occur, but are most often postnatal. 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), • 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. 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. Facial features Several characteristic craniofacial abnormalities are often visible in individuals with FAS. 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. 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. 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, 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. 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: • 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 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. 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. All four diagnostic systems allow for assessment of CNS damage in these areas, but the 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. 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. 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. 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. Neurological 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. 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. 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. Alcohol exposure 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, 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: • Confirmed exposure: The CDC guidelines are silent on using information on the 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 30 days. "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. 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 trimesters since this is when the meconium begins to form. Concentrations of FAEE can be influenced by medication use, diet, and individual genetic variations in FAEE metabolism, however. Differential diagnosis 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: • Attention deficit hyperactive disorder • Autism spectrum disorder • Reactive attachment disorder • Oppositional defiant disorder • Sensory integration dysfunction • Bipolar disorder • Depression Most people with FASD have most often been misdiagnosed with ADHD due to the large overlap between their behavioral deficits. ==Treatment==

Although the condition has no available cure, treatment can improve outcomes. Because central nervous system damage, symptoms, secondary disabilities, and needs vary widely by individual, there is no one treatment type that works for everyone. Medications 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. Behavioral interventions are based on the learning theory, which is the basis for many parenting and professional strategies and interventions. 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. 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. Treating FAS at the public health and public policy level promotes FAS prevention and diversion of public resources to assist those with FAS. 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 obstetrics and gynaecology 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. ==Prognosis==

The prognosis of FASD is variable depending on the type, severity, and whether treatment is issued. Prognostic disabilities are divided into primary and secondary disabilities. Primary disabilities The primary disabilities of FAS are the functional difficulties with which the child is born as a result of central nervous system damage due to prenatal alcohol exposure. Often, primary disabilities are mistaken as behavior problems, but the underlying central nervous system damage is the originating source of a functional difficulty, 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. • Impaired motor development and functioning are associated with reduced size of the cerebellum • Hyperactivity is associated with decreased size of the corpus callosum Functional difficulties may result from CNS damage in more than one domain, but common functional difficulties by domain include: Note that this is not an exhaustive list of difficulties. • Achievement: Learning disabilities • Adaptive behavior: Poor impulse control, poor personal boundaries, poor anger management, stubbornness, intrusive behavior, too friendly with strangers, poor daily living skills, developmental delays • Attention: Attention-deficit/hyperactivity disorder (ADHD), poor attention or concentration, distractible • Cognition: Intellectual disability, confusion under pressure, poor abstract skills, difficulty distinguishing between fantasy and reality, slower cognitive processing • Executive functioning: Poor judgment, information-processing disorder, poor at perceiving patterns, poor cause and effect reasoning, inconsistent at linking words to actions, poor generalization ability • Language: Expressive or receptive language disorders, grasp parts but not whole concepts, lack understanding of metaphor, idioms, or sarcasm • Memory: Poor short-term memory, inconsistent memory and knowledge base • Motor skills: Poor handwriting, poor fine motor skills, poor gross motor skills, delayed motor skill development (e.g., riding a bicycle at an appropriate age) • Sensory processing and soft neurological problems: sensory processing disorder, sensory defensiveness, undersensitivity to stimulation • Social communication: Intrude into conversations, inability to read nonverbal or social cues, "chatty" but without substance Secondary disabilities The secondary disabilities of FAS are those that arise later in life, secondary to central nervous system 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. 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): • 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 incarceration 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: • 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 Eight factors were identified in the same study as universal protective factors that reduced the incidence rate of the secondary disabilities: • 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 interest and talents as strengths that often stand out for those with FASD and should be utilized, like any strength, in treatment planning: • Music, playing instruments, composing, singing, art, spelling, reading, computers, mechanics, woodworking, skilled vocations (welding, electrician, etc.), writing, poetry • Participation in non-impact sports or physical fitness activities Lifespan One study found that the people with FAS had a significantly shorter life expectancy. 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. ==Epidemiology==

Globally, one in 10 women drinks alcohol during pregnancy. Out of this population, 20% binge drink and have four or more alcoholic drinks per single occasion. Australia FASD among Australian youth is more common in indigenous Australians. The only states that have registered birth defects in Australian youth are Western Australia, New South Wales, Victoria and South Australia. Passive surveillance is a prevention technique used within Australia to assist in monitoring and establishing detectable defects during pregnancy and childhood. Canada A 2015 review article estimated the overall costs to Canada from FASD at $9.7 billion (including from crime, healthcare, education, etc.). South Africa In South Africa, some populations have rates as high as 9%. 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%). 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. FASD is estimated to affect between 1–2% and 5% of people in the United States and Western Europe. 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. 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. ==History==

Before designation Some hold that ancient sources describe the negative effects of alcohol during pregnancy, identifying admonitions from ancient Greece, Rome, the Talmud, and the Bible. 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. , 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". There are many other such historical references during that period. 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. including the teratogenic effects of alcohol on animal embryos, This contradicted the predominant belief at the time that heredity caused intellectual disability, poverty, and criminal behavior, which contemporary studies on the subjects usually concluded. though later researchers have suggested that the Kallikaks almost certainly had FAS. General studies and discussions on alcoholism throughout the mid-1900s were typically based on a heredity argument. 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. 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." Vomiting put the mother at a high risk for aspiration and was "a brutal procedure for all involved". Recognition as a syndrome 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. In 1968, Paul Lemoine of Nantes published a study in a French medical journal about children with distinctive features whose mothers were alcoholics. 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. This study is arguably the true source of the modern understanding. 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. 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. 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. 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. In 1996, the replacement terms alcohol-related brain damage (ARBD) and alcohol-related neurodevelopmental disorder (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 1990s, fetal alcohol spectrum disorder (FASD), was adopted, 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. Alcohol-related birth defects (ARBD), formerly known as possible fetal alcohol effect (PFAE), The IOM presents ARBD as a list of congenital anomalies that are linked to maternal alcohol use but have no key features of FASD. In 2013, the American Psychiatric Association introduced neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE). ==Society and culture==

Criminalization Criminalization of substance use during pregnancy because of harm to the fetus or child is fiercely debated. Elizabeth Armstrong has questioned the zero-tolerance approach taken towards alcohol consumption during pregnancy, describing it as a moral panic. 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 (cf. ). Tennessee's 2014 fetal assault law (which expired in 2016) was criticized for not addressing alcohol use. The law criminalized opioid use during pregnancy and resulted in women avoiding professional medical care for fear of prosecution. A wide variety of professional organizations oppose criminalization. Minnesota, North Dakota, Oklahoma, South Dakota, and Wisconsin have statutory authorization for the involuntary civil commitment of women who abuse alcohol during pregnancy. 2016 CDC controversy In 2016, a CDC press release and infographic entitled "More than 3 million US women at risk for alcohol-exposed pregnancy" caused controversy. The CDC release contained the message "The risk is real. Why take the chance?". Darlena Cunha of Time 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". Julie Beck said that the infographic insinuated that "your womb is a Schrödinger'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". The CDC later clarified that the infographic was not intended to make any new guidelines or recommendations for women who are not pregnant, but rather to encourage conversations about alcohol with health professionals. Nonetheless, half of all pregnancies in developed countries and over 80% in developing countries are unplanned. Many women do not realize they are pregnant during the early stages and continue drinking when pregnant. In fiction 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. ==See also==