It is a shame that in today’s "enlightened" society so many preventable diseases and disorders are still occurring. Fetal alcohol syndrome is one of these totally preventable disorders. It is one of the most frequent and important causes of mental and physical retardation in childhood today.

Only in the past decade or so have scientists identified and named this disorder. However, effects of alcohol consumption during pregnancy have been suspected for quite some time. In the Old Testament the wife of Menoh is warned not to drink alcoholic beverages during pregnancy (Judges 13, 2-25).

Despite all the current information about the negative effects of alcohol consumption during pregnancy, many people are still unaware of the complications it can cause. In one study it was found that students were aware that alcohol is a teratogenic substance, but had little knowledge as to the nature and timing of the possible negative side effects that alcohol consumption at each stage might cause (Haemmerlie, 1992).

Besides those who are unaware of the results of alcohol consumption during pregnancy, there are also those women who are aware of the consequences, but don’t care enough or have enough willpower to stop. These alcoholic mothers may know the consequences of drinking during pregnancy but are unable to stop themselves.

The effects of prenatal exposure to alcohol may have a wide range of possible effects; from life--threatening anomalies to mild problems with attention and learning. There are many symptomology’s that are characteristic of FAS children. The diagnosis of FAS can only be made when the patient has at least one abnormality in each of three categories (Sokol & Clarren, 1989): pre- and post-natal growth retardation, typical crainio-facial malformations, and central nervous involvement.

Growth retardation is evident in length, weight, and head circumference. Crainio-facial malformations include short palpebral fissures, a poorly developed philtrum, thin upper lip vermillion, short mandibles, a flattened midface structure, and dysplastic ears. Central nervous system involvement is evidenced by mental retardation. Ophthalmological symptoms are present in 90% of FAS children also. These include myopia, ptosis, epicanthus, hypoplasia of optic disc, and torturous retinal vessels.

Besides intellectual impairment, FAS children sometimes also suffer from attention deficits. One study measured four different areas of attention. The results of the FAS children, though significantly more intellectually impaired, correlated strongly in the other three areas with children diagnosed with Attention- Deficit Disorder (Nanson & Hiscock, 1990). These finding are important in that treatment methods developed for ADD children may also be useful in treating FAS children who have an attention deficit.

Autism may also be a disease caused by alcohol exposure of the fetus during pregnancy. Autistic children diagnosed with fetal alcohol syndrome generally demonstrated a greater degree of mental and growth retardation, as well as a greater number of anomalies. This information tends to suggest that these children suffered a greater degree of alcohol exposure, as compared with non-autistic FAS children (Nanson, 1992).

One other disorder, just recently thought to be caused by prenatal exposure to alcohol, may be schizophrenia. Evidence is growing which implicates prenatal alcohol exposure as an etiological agent for schizophrenia and may relate to a small fraction of FAS children who go on to develop this disease later in life (Lohr & Bracha, 1989).

There are many theories as to how the alcohol exposure causes these wide-ranging symptoms. Much research is still being done in this area. One hypothesis, by Pullerkat, implicates retanoic acid in the central nervous system disorders and limb abnormalities. Two main reasons support his theory. One is because retinoic acid and didehydroretinoic acid has been shown to play a central role in the development of the limbs and of the central nervous system. The second reason is that ethanol inhibits the formation of retinoic acid from retinal, as well as depletes the levels of hepatic retinoid. Pullerkat believes that these low levels of retinoic acid induced by fetal alcohol exposure is responsible for the aforementioned developmental defects (1991).

Another theory links the alcohol-induced brain damage to glutamate-induced excitotoxicity which is driven by nitric oxide. Lancaster has found that an increased number of glutamate binding sites and calcium membrane channels are present on the hippocampal and cerebellar neurons after chronic alcohol abuse. It occurs primarily in the cerebellum because it contains the greatest concentration of nitric oxide synthase. The synthase is also active in the cortex, caudate nuclei, putamen, basal forebrain, dentate gyrus of the hippocampus, supraoptic nuclei, and the superior and inferior colliculus. Lancaster believes alcohol disturbances in these areas cause changes in learning memory, vision, balance, and modulation of food and drink intake (1992).

Many techniques are being used to help us see which areas of the brain are affected. One study uses magnetic resonance imaging and electroencephalograms to study FAS patients. The MRI’s showed abnormalities in the corpus callosum and reduction in the size of the basal ganglia and thalamic structures. The EEG’s were abnormal, but no focal point was obvious in these readings (Mattson et. al., 1992).

Now that the symptoms and some theories of the causes of fetal alcohol syndrome are a little more clear, the question remains: What can be done to prevent it?

Pregnant women whose alcohol use exceeds 3-5 drinks per day have a 30-50% chance of delivering a child with fetal alcohol defects. This could be prevented if the women were counseled and if they decreased their drinking. One way to detect alcohol abuse during pregnancy that is being tested is use of acetaldehyde--hemoglobin (Hb-Ach) adducts. By using an antiserum specific for the acetaldehyde generated protein epitomes, levels of Hb-Ach from the red blood cells can be measured. The highest concentrations of Hb-Ach have been found in women who subsequently delivered children with fetal alcohol defects. As well as supporting a role of acetaldehyde in producing FAS, these measurements may provide a way of monitoring the compliance of pregnant women in withdrawing from alcohol and also to distinguish the mothers at risk of delivering affected offspring (Niemele, Halmesmak & Ylikorkala, 1991).

Education of the population as to the specific effects of alcohol use during pregnancy is really the only method of prevention society has. So what happens when children with FAS are born?

If the addicted families remain untreated, the infants and children raised be these families run a high risk of abuse and/or neglect (Bays, 1992). Early intervention and ongoing supervision may be necessary to break the multigenerational cycle of both diseases. If we cannot prevent FAS from occurring, the least we can do for these children who are already victims of substance abuse, is to prevent them from also being victims of child abuse.

REFERENCES:

Bays, J. "The care of Alcohol- and Drug-Affected Infants". Pediatric Annals, Vol. 21, Aug. 1992, pp. 485-495.

Haemmerlie, F. M., Mere, C. J., & Nelson, S. B. "College vs Junior High School Students’ Knowledge of Alcohol as a Teratogen". Psychological Reports, Vol. 71, No. 3.1, Dec. 1992, pp. 809-910.

Lancaster, F. E. "Alcohol, Nitric Oxide and Neurotoxicity: Is There a Connection?" Alcoholism, Vol. 16, No. 3, pp. 539-541.

Lohr, J. B., & Bracha, H. S. "Can schizophrenia be Related to Prenatal Exposure to Alcohol? Some Speculations". Schizophrenia Bulletin, Vol. 15, No. 4, 1989, pp. 595-603.

Mattson, S. N. et. al. "Fetal Alcohol Syndrome: A Case Report of Neuropsychological, MRI, and EEG Assessment of Two Children". Alcoholism, Vol. 16, No. 5, Oct. 1992, pp. 1001-1003.

Nanson, J. L. "Autism is F.A.S. - A Report of Six Cases". Alcoholism, Vol. 16, No. 3, May/June 1992, pp. 558-565.

Nanson, J. L., & Hiscock, M. "Attention Deficits in Children Exposed to Alcohol Prenatally". Alcoholism, Vol. 14, No. 5, Oct. 1990, pp. 656-661.

Niemele, O., Helmesmaki, E., & Ylikorkala, O. "Hemoglobin--acetaldehyde Adducts are Elevated in Women Carrying Alcohol-damaged Fetuses". Alcoholism, Vol. 15, No. 6 ,Dec. 1991, pp. 1007-1010.

Old Testament, Judges 13, 2-25.

Pullerkat, R. K. "Hypothesis: Prenatal Ethanol-induced Birth Defects and Retanoic Acid". Alcoholism, Vol. 15, No. 3, June 1991, pp. 565-567.

Sokol, R. J. & Clarren, S. K. "Guidelines for Use of Terminology Describing the Impact of Prenatal Alcohol on the Offspring". Alcoholism, Vol. 13, No. 4, July/August 1989, pp. 597-598.