Fetal alcohol syndrome (FAS) and Fetal Alcohol Spectrum Disorders (FASD) describes the range of disorders caused by prenatal alcohol exposure to the developing fetus(BMA Board of Science, 2007; Warren & Foudin, 2001; Warren, Hewitt & Thomas 2011). FASD is an overarching umbrella term encompassing the behavioural diagnoses but when the full phenotype of FAS has not developed. The spectrum of FASD incudes a range of diagnoses from Full Fetal Alcohol Syndrome to Alcohol Related Neurodevelopmental Disorder (ARND). The latter describes the damage caused to the developing brain by alcohol without the other features(BMA Board of Science, 2007; Warren, Hewitt & Thomas, 2011).

Fetal Alcohol Syndrome (FAS) was first reported in the international literature by Jones and Smith in 1973 ( Jones & Smith, 1973; Jones, Smith, Ulleland, & Streissguth, 1973). Prior to that Lemoine published a series of 127cases in France highlighting the phenotypic presentation of people exposed to alcohol whilst pregnant (Lemoine, Harousseau, Borteryu, & Menuet, 1968). The full syndrome is characterised by a combination of short stature, neurocognitive deficits and a specific triad of facial dysmorphology (short palpebral fissures, flat philtrum and thin upper lip vermilion)(BMA Board of Science, 2007).

Over the last 30 years the opinions of professionals working in this field have changed. Previously FAS was considered to be a possible consequence of chronic alcohol consumption occurring in specific high-risk populations (such as the native American Indian tribal groups)(Warren & Foudin, 2001) The term FAE (fetal alcohol effects) started to become used more widely(Aase, Jones, & Clarren, 1995). This related to children who were exposed to heavy alcohol exposure at times where facial characteristics or the growth would not be present but cognitive features would remain. Views later changed to encompass moderate consumption in all populations(Warren & Foudin, 2001). Biological, animal and now human evidence is providing confirmation that behavioural changes in a child with FASD may be seen even at low doses of alcohol consumption(Cudd, 2005; Hannigan, 1996).

Aase, J. M., Jones, K. L., & Clarren, S. K. (1995). Do we need the term "FAE"? Pediatrics, 428-430. BMA Board of Science (2007). Fetal Alcohol Spectrum Disorders, a guide for healthcare practitioners London: BMA Publishing. Cudd, T. A. (2005). Animal model systems for the study of alcohol teratology. Experimental Biological Medicine, 230, 389-393. Hannigan, J. H. (1996). What research with animals is telling us about alcohol-related neurodevelopmental disorder. Pharmacology, Biochemistry & Behavior.55(4):489-99. Jones, K. L. & Smith, D. W. (1973). Recognition of the Fetal Alcohol Syndrome. Lancet, 999-1001. Jones, K. L., Smith, D. W., Ulleland, C., & Streissguth, A. P. (1973). Patterns of malformations in offspring of chronic alcoholic mothers. Lancet, 1267-1271. Lemoine, P., Harousseau, H., Borteryu, J. P., & Menuet, J. C. (1968). les enfants des parents alcoholiques: anomoloies observees a propos de 127 cas. Quest Medical, 25, 482. Warren, K.R., Hewitt, B.G., Thomas, J.D. (2011) Fetal Alcohol Spectrum Diosrders: Research Challenges and Opportunities. Alchol Researchand Health 34(1), 4-14. Warren, K. R. & Foudin, L. L. (2001). Alcohol-related birth defects: the past, present and future. Alcohol Research & Health, 25, 153-158.