Treatment and Prevention of FAS

Due to the nature of FAS and the damage it inflicts to the Central Nervous System, it creates a permanent disability. Though there are measures of treatment available, there is no cure, nor does any single treatment work for everyone.[3] The treatment for FAS may occur prenatally or after the birth of the child. When providing treatment during in utero stages, it gives the opportunity to prevent, slow or reverse the damages that are associated with alcohol during the prenatal period. In order to provide treatment in prenatal stage, early recognition of alcohol exposure to the fetus is crucial.[10]

Alcohol is known to cause neurodegeneration in rat brain. It has the same effect as gamma-aminobutyric acid (GABA) specific agonists. The consumption of alcohol does not fully explain FAS. Factors such as malnutrition alongside exposure to alcohol increases susceptibility to FAS. It has been illustrated that 40% of infants born to mothers of the lower socioeconomic status were diagnosed with FAS compared to 2.7% of infants born to middle class alcoholics. Individuals that are living under poverty lines are at greater risk of developing micronutrients and macronutrients deficiencies. Health authorities have determined that alcoholism and malnutrition have a contributing factor to folic and cholic deficiencies. [1] Proteins, certain types of fats, iron, zinc, iodine, vitamin A, and choline are significant in fetal development especially with regards to brain and neurobehavioural functions.[3]



There are many potential benefits to prenatal treatment. It gives the opportunity to stop, slow down, or reverse any damages that may occur during this period. Such treatments require early detection; however, there are no treatments that are currently certified and ready for clinical use. Proposed treatments target the mechanisms that mirror such induced damage. To counter the oxidative stress of ethanol in animal models, Vitamin C, E, and green tea extracts (antioxidants) have been used. Due to the nature of the effects on the brain, prenatal treatments are largely at their infancy.[10] Providing supplementation of folate, choline and vitamin A to mothers can lessen the effect of alcohol in the utero stage and help in eliminating the most common neurodevelopmental disorders associated with fetal alcohol syndrome. [1]

Choline plays a role inside the extracellular environment by functioning as a precursor to acetylcholine and the developing brain. Acetylcholine is used as a growth factor and has been implicated in both gastrulation and neurulation. It has been established that rats which are exposed to ethanol in utero and given choline as a supplement have decreased effects of ethanol on development and behaviour.[1]

Vitamin A

Studies have found that vitamin A deficiency impair memory and long term potentiation in mice.[1] Retenoic Acid (RA) is an oxidative metabolite in vitamin A. Its major role in embryonic development is through acting on the cells to establish or change the pattern of gene activity.[7] Alcohol is considered to have direct effects on retinoic acid metabolism either through the direct inhibition of alcohol or acetaldehyde dehydrogenase. The inhibition decreases the amount of retinoic acid needed to produce the effects of neural development. Administration of vitamin A or retinoic acid during gastrulation has shown to significantly decrease birth defects that are caused by ethanol.[1]

Serotonin agonists

Novelty-Surpressed Feeding Test
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Fig1. Adapted from Marche et al. [2010] [8]. Measures latency of feeding for control and ethanol groups

Studies indicate that serotonin agonist(5-HT 1A) such as buspirone and ipsapirone can be used for the treatment of brain malformations caused by prenatal ethanol exposure.[11] Serotonin modulates certain functions such emotion, cognition, circadian and motor activity. Any imbalance will result in a wide spectrum of dysfunctions including mood swings, anxiety, insomniac etc.[12] When ethanol is fed to pregnant rats, the development of serotonin (5-HT) and S100B- immunopositive glia neurons are impaired. Ethanol can also compromise the vulnerable period in the development of serotonin (5-HT) and potentially cause serious damage to the developing 5-HT system. Treatment with 5-HT agonist such as buspirone and ipsapirone during the gestational days 13-20 prevents most of the ethanol- associated damages to the developing 5-HT and S100B-immunopositive glia neurons in offspring.[4]



A study using rat models was able to show that the administration of transient fenofibrate on young rats that were exposed to alcohol was able to reduce pre- and post-pubertal hyperactivity. With two samples, one being exposed to alcohol and one not treated and administrating fenofibrate, it was found that there was partial effect on anxiety as seen through the prevention of attention deficit during the hyperactive phase. In one case (Fig 1.) both groups were administered the Novelty-Suppressed Feeding test. The onset to feeding for rats with ethanol against controls was significant[8] The study is vital to understanding the possible pharmacological modulation of nuclear receptors that would lead to a therapeutic method of treating this disorder.


The First Step to Treatment is Prevention

Alcohol Abstinence

Alcohol is known to act as a teratogen. Research done by the Centers of Disease Control and Prevention have shown that there is no safe period of time during pregnancy to consume alcohol; thus, women who are pregnant should abstain from alcohol.[6] The rate of alcohol use among pregnant women, despite the number of campaigns and warning outlining the implications, is quite high. Though treatment is an alternative, the most effective means of reducing cases of FAS is through public health intervention as well as prevention of alcohol use while pregnant. Various studies have been used to assess the effectiveness of interventions in reducing the consumption of alcohol when paired with a partner.[10] Chang’s (2005) study used randomized trials using 304 pregnant women and their partners were assessed. Pregnant women with a positive T-ACE (Tolerance, Annoyed, Cut down, Eye-opener) were at risk for consumption of alcohol during pregnancy. Factors that led to prenatal alcohol consumption were less awareness through education, social temptations, and history of drinking more alcohol in proportion to a period of time. The level of confidence was seen to contribute to more control in social situations.[2]

Growth Retardation

Other studies have assessed the risk of newborns and the correlation to drinking, particularly the effects of alcohol in proportion to the birth weight of a newborn. Since the intrauterine growth retardation was reported as a cause of FAS, the correlation between growth and ethanol in a mother’s body has become an increasing concern.[5] A study examining over 34,000 prospective mothers was undertaken to understand the minimal threshold before it took a notable effect. When subjects were assessed, it was found that that heavy drinkers were less educated, concurrently smoking, blacks, and Hispanic. The data was adjusted for the mean given many heavy drinkers were smokers, and this confounding variable was also a reason for lower birth weight cases.[9]

1. Ballard, M. S., Sun, M., & Ko, J. (2012). Vitamin A, folate, and choline as a possible preventive intervention to fetal alcohol syndrome. Medical hypotheses, 78(4), 489-493.
2. Chang, Grace., McNamara, Tay K., Orav, John E. et al. (2005). Brief Intervention for Prenatal Alcohol Use: A Randomized Trial. Obstet Gynecol. 105(5 Pt 1)L 991-998.
3. DeRegnier, R. A., & Desai, S. (2010). Fetal development. Wiley-Blackwell Handbook of Infant Development, 2 (2nd edition).
4. Erikson, J. L., & Druse, M. J. (2001). Astrocyte- mediated tropic support of developing serotonin neurons: effects of ethanol, buspirone and S100B. Developmental Brain Research, 131: 9-15.
5. Floyd, R. L., O'Connor, M. J., Sokol, R. J., Bertrand, J., & Cordero, J. F. (2005). Recognition and prevention of fetal alcohol syndrome. Obstetrics & Gynecology,106(5, Part 1), 1059-1064.
6. Ismail, S., Buckley, S., Budacki, R., Jabbar, A., & Gallicano, I. A. (2010). Screening, diagnosing and prevention of fetal alcohol syndrome: Is this syndrome treatable?. Developmental Neuroscience, 32(2): 91-100.
7. Maden, M. (2000). The role of retinoic acid in embryonic and post-embryonic development. The Proceeding of Nutrition Society, 59 (1): 65-73.
8. Marche, K., Danel, T., & Bordet, R. (2011). Fetal alcohol-induced hyperactivity is reversed by treatment with the PPARα agonist fenofibrate in a rat model. Psychopharmacology, 214(1): 285-296.
9. Mills JL, Graubard BI, Harley EE, Rhoads GG, Berendes HW. (1984). Maternal Alcohol Consumption and Birth Weight: How Much Drinking During Pregnancy Is Safe JAMA.1984; 252(14): 1875-1879.
10. Pruett, D., Hubbard Waterman, E., Caughey, A.B. (2013) Fetal Alcohol Exposure: Consequences, Diagnosis, and Treatment. Obstetrical and Gynecological survey. 68(1): 62-69.
11. Zhou FC, Sari Y, Li TK, Goodlett C, Azmitia EC (2002): Deviations in brain early serotonergic development as a result of fetal alcohol exposure. Neurotox Res 4: 337–342.
12. Zhou FC, Sari Y, Zhang JK, Goodlett C, Li T. (2001): Prenatal alcohol exposure retards the migration and development of serotonin neurons in fetal C57BL mice. Dev. Brain Res 126:147-155.

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