Diseases and Disorders

Fetal Alcohol Syndrome: A Few Drinks Can Hurt

Megumi Sano


Ancient Greek and Roman writings show that newlyweds were forbidden to drink on their wedding night. Aristotle (384 - 322 BC) believed in the association between alcohol consumption during pregnancy and congenital abnormalities, describing the children of “drunken women” as “morose and languid” (Mitchell et al.). Fast-forward two millennia: in 1968 France, the first paper was published on the shared abnormalities of 127 children born to alcoholic mothers, identifying alcohol as a teratogen, an agent that can disturb embryo or fetus development (Lemoine et al.). Described as fetal alcohol syndrome five years later (Jones et al.), FAS has been the leading non-genetic cause of mental retardation. Many argue that children born with the syndrome are denied their rights to health and normal development, as interventions may only alleviate but never eliminate their symptoms. Nevertheless, alcohol use has been self-reported by approximately 15% of pregnant women in the United States with rates as high as 20% in recent decades (National Household Survey), which communicates the need for a greater level of awareness.

Overview and Symptoms

    Fetal Alcohol Syndrome (FAS) is one of the specific diagnostic categories used under the umbrella term, Fetal Alcohol Spectrum Disorders (FASD). While FASD refers to the range of effects that can occur in an individual who is exposed to alcohol during the nine month prenatal period before birth, FAS indicates the most severe end of the spectrum, with fetal death being the most extreme outcome (Center for Disease Control and Prevention). Recent reports show the prevalence of FASD to be as high as 20 to 70 cases per 1000 live births (May et al.), while that of FAS is 2 to 7 cases per 1000 (Stratton et al.). Symptoms of FAS include a constellation of abnormal facial features, small head circumference, short height, weak immune system, hearing and vision problems, memory problems, and lack of focus or hyperactivity. However, the effects of FAS on the child depend heavily upon the mother’s alcohol consumption in different stages of pregnancy. The general trend is that alcohol consumption leads to more severe brain damage in later stages of pregnancy. For example, children with mothers who consumed alcohol during the first trimester of their pregnancy statistically experience more facial malformation and damaged organs.  Contrarily, those exposed to alcohol in the second or third trimester may encounter destruction of brain cells and therefore impairment of the final stages of brain development. This may result in more functional problems than physical abnormalities. Symptoms of FAS do not fade after childhood; its long-term consequences feed into adolescence and adulthood and may include social withdrawal, impulsive behavior, and aggression. In fact, very few adults with FAS are able to live and work independently, with significantly higher rates of mental illness, psychosis, sexual and social problems, suicide, and drug and alcohol abuse (Spohr).


    Often, the main cause of FAS is misunderstood. It is believed by many to be excessive alcohol consumption by pregnant mothers. However, the term “excessive” is unnecessary, as there is no particular threshold of alcohol use for the child to develop symptoms of FAS. Any pregnant woman drinking alcohol during pregnancy has a significantly higher risk of giving birth to a child with FAS than those who entirely avoid alcohol. It is also important to acknowledge that alcohol concentration and therefore the type of alcohol consumed does not determine manifestation of the disorder, much less the severity of the disorder. There are many other factors, such as the mother’s digestive system, contributing to the severity of FAS; outcomes of alcohol consumption during pregnancy are unique to the individual. In terms of biological mechanisms, the primary reason behind alcohol’s destructive influence on the fetus’s development is the difference in abundance and efficiency of the enzymes responsible for breaking down alcohol in the liver of the mother and fetus.



    Currently, there is no approved medical test for diagnosing FAS. Doctors will normally look for the following signs: 1) abnormal facial features which may include thin upper lip, smooth philtrum, and small eye openings, 2) growth problems indicated by height and weight, and 3) central nervous system problems which may be classified into structural, neurological, and functional (“Centers for Disease Control and Prevention,” 2014). Structural problems of the central nervous system mainly refer to reduced head circumference or significant changes in brain structure, while examples of peripheral nervous system  problems include poor muscle control that indicate impaired nerve transmission. Some of the major functional problems are cognitive deficits, executive functioning deficits, motor functioning delays, problems with attention, impaired social skills, and impaired hearing and vision. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) is presently aiming to create a new set of criteria for recognizing alcohol-related neurodevelopmental disorder (ARND), which is a diagnostic term on the milder end of FASD.  In turn, the diagnostic criteria specific for FAS, which is on the more severe end of the spectrum, also need further improvement as doctors are fully dependent upon them to make consequential diagnostic decisions. Interestingly, although doctors may also check for prenatal exposure to alcohol through a questionnaire by the mother, this is not a requirement. In other words, if the child meets all the other three criteria listed above, confirmation of the mother’s alcohol consumption during pregnancy is not necessary for diagnosis, despite it being the main cause of FAS.



     Alcohol is the most common human teratogen, meaning that it has the potential to induce physical and behavioral effects on the fetus. There is an unimpeded bidirectional movement of alcohol between maternal and fetal tissue, resulting in equal alcohol concentrations after the mother’s consumption. Since an enzyme called alcohol dehydrogenase (ADH) in the fetal liver shows less than 10% of the activity it shows in the adult liver, the fetus cannot detoxify alcohol on its own and experiences intensified impacts by the same alcohol concentration. Moreover, the amniotic fluid surrounding the fetus may act as an alcohol store, decreasing metabolism and further prolonging alcohol’s harmful effects. Although some molecular mechanisms are still unknown, research suggests an array of potential mechanisms including disruption of cellular differentiation and growth, interference with DNA and protein synthesis, decrease in serotonin levels, and inhibition of cell-to-cell adhesion. One of the most frequently proposed of these mechanisms is the blockage of N-methyl-d-aspartate (NMDA) receptors. Alcohol interacts with a number of neuronal membrane receptors including NMDA receptors which play an important role in neuronal plasticity during development and later in life. Chronic blockage of these receptors may lead to adaptive upregulation during periods of withdrawal, increasing either receptor number or the release of glutamate, the excitatory neurotransmitter that usually activate these receptors. As a result, NMDA receptors are overactivated and this eventually leads to excitotoxic cell death. This chain of processes can occur during fetal development (Irdus & Thomas) and it is this cell loss that hugely contributes to symptoms of FAS.

     Currently, neuroimaging is also used to identify damaged parts of the  brain and their relationship with neurocognitive and behavioral symptoms in children with FAS. While one paper indicated an association between decreased volume of the caudate nucleus and impaired cognitive performance and verbal learning (Fryer et al.), another has concluded a correlation between reduced palpebral fissure length and neurocognitive impairment (Yang et al.). These studies help to enhance our understanding of the bigger picture without solely focusing on molecular pathophysiology.



    Although there are currently no cures available for FAS, early intervention and treatment services may support the child’s development and alleviate its negative effects on quality of life. Parents and guardians have the option of choosing between a wide range of services including behavior therapy, speech therapy, parent training, and alternative educational pathways, which may not only reduce the child’s functional symptoms but also create a suitable environment for each individual’s learning capabilities. In addition, some medications for the pregnant mother have shown potential therapeutic properties including antioxidants which mitigate the effects of alcohol exposure on the imbalance of the intracellular reduction-oxidation state (Joya et. al, 2015). These can be taken as food supplements during the prenatal period by the mother. However, discouraging alcohol consumption during pregnancy is the most effective approach to reducing risks of FAS and securing the basic human rights of innocent children.


Further Reading

National Organization on Fetal Alcohol Syndrome www.nofas.org

Rodriguez, J. and Kaur, N. (2016). Fetal Alcohol Syndrome Affects in Retinal Cell Gene Expression. Poster session presented at IUPUI Research Day 2016, Indianapolis, Indiana.

Roozen, S., Peters, G., Kok, G., Townend, D., Nijhuis, J., and Curfs, L. (2016). Worldwide Prevalence of Fetal Alcohol Spectrum Disorders: A Systematic Literature Review Including Meta-Analysis. Alcoholism: Clinical and Experimental Research. 18-32.



Adaptive upregulation - An increase of a cellular component such as the number of receptors to a molecule in response to molecular stimulus which enhances the cell’s sensitivity to the molecule.

Alcohol dehydrogenase (ADH)- A group of enzymes that facilitate the interconversion between alcohols and aldehydes or ketones with the reduction of nicotinamide adenine dinucleotide (NAD+).

Alcohol-related neurodevelopmental disorders (ARND) - A complex range of disabilities in neurodevelopment and behavior, adaptive skills, and self-regulation in the presence of confirmed prenatal alcohol exposure. Unlike those with FAS, children with ARND do not have abnormal facial features or growth problems.

Antioxidant - Any agent that inhibits oxidation by removing oxidizing agents.

Caudate nucleus- The upper of the two gray nuclei of the corpus striatum in the cerebrum.

Cell-to-cell adhesion- The process by which cells interact and attach to a surface, substrate, or another cell, mediated by interactions between transmembrane glycoproteins.

Excitotoxic cell death -  The death of neurons arising from prolonged exposure to glutamate and the associated excessive influx of ions into the cell.

Fetal Alcohol Syndrome (FAS)- A congenital syndrome associated with alcohol consumption by the mother during pregnancy and characterized by physical and mental abnormalities.

Fetal Alcohol Spectrum Disorders (FASD)- A group of conditions that can occur in an individual whose mother drank alcohol during pregnancy. This includes fetal alcohol syndrome (FAS), alcohol-related neurodevelopmental disorder (ARND), partial fetal alcohol syndrome (pFAS), and neurobehavioral disorder associated with prenatal alcohol exposure (NP-PAE).

Glutamate- An excitatory neurotransmitter involved in learning and memory.

N-methyl-d-aspartate (NMDA) receptor- An ionotropic glutamate receptor that allows positive charged ions to flow into the cell when activated by glutamate or glycine.

Palpebral fissure - The elliptic space between the medial and lateral canthi of the two eyelids; the distance between the inner and outer corners of the eye.

Philtrum- The vertical groove between the base of the nose and the border of the upper lip.

Serotonin - A neurotransmitter involved in the control of pain perception, the sleep-wake cycle, and mood.

Teratogen - Any agent that can disturb the development of an embryo or fetus and may cause birth defects and congenital disorders.


  1. Joya, X., Garcia-Algar, O., Salat-Batlle, J., Pujades, C. and Vall, O. (2015). Advances in the development of novel antioxidant therapies as an approach for fetal alcohol syndrome prevention. Birth Defects Research Part A: Clinical and Molecular Teratology. 163–177.

  2. Yang, Y., Roussotte, F., Kan, E., Sulik, K. K., Mattson, S.N., Riley, E.P., Jones, K.L., Adnams, C.M., May, P.A., O’Connor, M.J., Narr, K.L. and Sowell, E.R. (2012). Abnormal cortical thickness alterations in fetal alcohol spectrum disorders and their relationships with facial dysmorphology. Cerebral Cortex. 1170-9

  3. Fryer, S. L., Mattson, S. N., Jernigan, T.L., Archibald, S.L., Jones, K.L. and Riley, E.P. (2012). Caudate volume predicts neurocognitive performance in youth with heavy prenatal alcohol exposure. Alcoholism: Clinical and Experimental Research. 1932-41.

  4. Irdus, N. and Thomas, J. (2011). Fetal Alcohol Spectrum Disorders: Experimental Treatments and Strategies for Intervention. Alcohol Research & Health Volume 34. Issue Number 1.

  5. Data and Statistics. Centers for Disease Control and Prevention (2016). Fetal Alcohol Spectrum Disorders. http://www.cdc.gov/ncbddd/fasd/data.html#ref

  6. Spohr HL. (1996). Fetal Alcohol Syndrome in Adolescence: Long-term perspective of children diagnosed in infancy. Alcohol, Pregnancy, and the Developing Child. National Academy Press. 175-9.

  7. Stratton, K., Howe, C., and Battaglia, F., (1996). Fetal Alcohol Syndrome: Diagnosis, Epidemiology, Prevention, and Treatment. National Academy Press. 17.

  8. May, P.A., Gossage, J.P., and Kalberg, W.O. (2015). Prevalence and characteristics of fetal alcohol syndrome and partial fetal alcohol syndrome in a Rocky Mountain Region City. Drug Alcohol Dependence. 118-127.

  9. Facts about FASDs. Centers for Disease Control and Prevention (2016). Fetal Alcohol Spectrum Disorders. http://www.cdc.gov/ncbddd/fasd/facts.html.

  10. US Dept Health Human Services, Substance Abuse and Mental Health Services Administration, Office of Applied Studies. (1995). National Household Survey on Drug Abuse, 1994.

  11. Jones, K.L., Smith, D.W., Ulleland C.N. and Streissguth, P. (1973). Pattern of malformation in offspring of chronic alcoholic mothers. Lancet. 1267-71.

  12. Lemoine, P., Harousseau, H., Borteyru, J.P. and Andmenuet, J.C. (1968). Les enfants de parents alcooliques: anomalies observees a proposos de 127 cas [Children of alcoholic parents: abnormalities observed in 127 cases]. Quest Medecine. 476-82.

  13. Mitchell, K., M.H.S., and L.C.A.D.C. (2016). Fetal Alcohol Syndrome and Other Alcohol Related Birth Defects: Identification and Implications. NADD Bulletin Volume IV Number 1. Article 4. http://thenadd.org/nadd-bulletin/archive/volume-iv/

Megumi Sano

Megumi Sano

This author has not yet uploaded a bio.