Alcohol and Pregnancy and the Foetal Alcohol Syndrome


Foetal alcohol syndrome is a specific pattern of birth defects caused by prenatal alcohol exposure. The syndrome's components include somatic growth restrictions, characteristic midface abnormalities and brain dysfunction. ‘Foetal alcohol spectrum disorders’ (FASDs) includes the broad range of offspring effects caused by prenatal alcohol exposure. Alcohol is a teratogenic drug to which the developing brain is particularly vulnerable. Alcohol induces brain injury and dysfunction in the offspring through a variety of mechanisms, one of the most important of which is neuronal death. Alcohol‐induced neurodevelopmental sequelae most often include learning disorders, attention deficits and behaviour problems. These deficits can range from mild to severe, depending on dose and timing of the alcohol exposure, maternal and foetal genetics and other conditions of exposure. Because alcohol use is so prevalent and because the developing brain is so vulnerable, FASD is the most important preventable cause of cognitive deficiency in the western world.

Key Concepts

  • Foetal alcohol syndrome (FAS) is a constellation of developmental abnormalities that results from maternal alcohol abuse during pregnancy.
  • Components of FAS include prenatal and postnatal growth restrictions, a characteristic set of midface abnormalities and central nervous system dysfunction.
  • ‘Foetal alcohol spectrum disorders’ (FASD) is an umbrella term that encompasses the full range of adverse effects of alcohol on the offspring.
  • Many children who were prenatally exposed to alcohol have FASD, which most commonly manifests as neurodevelopmental problems, without having the full FAS syndrome.
  • The brain is the most vulnerable of the foetal organs to alcohol‐induced damage.
  • Alcohol damages the developing brain in a variety of ways, one of the most important of which is neuronal death.
  • The vulnerability of developing neurons to alcohol‐induced injury depends on a variety of factors, including the dose and timing of alcohol exposure.
  • Not all foetuses are equally vulnerable to alcohol‐induced injury; some possess certain genes that can increase or decrease their susceptibility to alcohol teratogenesis.
  • The most common neurodevelopmental problems induced by prenatal alcohol exposure are learning disorders, attention deficits and behaviour problems.
  • People with FASD are often particularly disabled by severe deficits in executive functions, a group of cognitive integrative behaviours that reflect the ability to self‐regulate, effectively plan, organise, keep focused on and carry out goal‐directed activity.

Keywords: foetal alcohol syndrome; foetal alcohol effects; birth defects; developmental disabilities; pregnancy outcome; alcohol

Figure 1. Brain regions most vulnerable to damage from prenatal alcohol exposure: (a) a human brain viewed from its medial surface; (b) a horizontal section of human brain at the plane corresponding to the line in (a). Prenatal alcohol exposure disrupts neuronal migration of the cerebral cortex (green), and changes the shape of the corpus callosum (blue), while it kills neurons in the hippocampus (red) and cerebellum (yellow).
Figure 2. FAS is only the ‘tip of the iceberg’ in terms of the proportion of people adversely affected by prenatal alcohol exposure. Many individuals prenatally exposed to alcohol lack the facial characteristics and somatic growth deficiencies of FAS, but can have brain dysfunction ranging from mild to severe, which can last for a lifetime.


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Further Reading

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Streissguth AP (1997) Fetal Alcohol Syndrome: A Guide for Families and Communities. Baltimore: Paul H. Brookes Publishing Company.

Streissguth AP and Kanter J (eds) (1997) The Challenge of Fetal Alcohol Syndrome: Overcoming Secondary Disabilities. Seattle: University of Washington Press.

West J (ed.) (1986) Alcohol and Brain Development. New York: Oxford University Press.

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Bonthius, Daniel J(Jul 2015) Alcohol and Pregnancy and the Foetal Alcohol Syndrome. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0002251.pub2]