Impaired neuropsychological development. Another study evaluating light to moderate amounts of prenatal alcohol exposure in 10- and 11-year-old children found significantly worse scores regarding a number of neuropsychological developmental assessments.24
No threshold dose of causation. Results of a 2012 prospective study in California, with data collected on 992 subjects from 1978 until 2005, revealed that many physical FAS features, including microcephaly, smooth philtrum, and thin vermillion border; reduced birth length; and reduced birth weight, were associated with alcohol exposure at specific gestational ages, and were dose-related.25 This paper didn’t reveal any evidence of a threshold dose of causation.
Neurobehavioral outcomes of FAS are not always considered
Another recent study that the media recently highlighted as finding “no association between low or moderate prenatal alcohol exposure and birth defects” was by O’Leary and colleagues.26 Like other similarly limited studies, this one involved only children younger than 6 years and didn’t assess any of the important neurobehavioral outcomes of FAS.
FAS encompasses much more than visible birth defects. As the aforementioned ACOG tool kit stated, “For every child born with FAS, many more children are born with neurobehavioral deficits caused by alcohol exposure but without the physical characteristics of FAS.”
The costs of FAS are felt with dollars, too
The financial cost to our nation is extraordinary. In 1991, Abel and Sokol estimated the incremental annual cost of treating FAS at nearly $75 million, with about three-quarters of that cost associated with FAS cases involving mental retardation.27
A 2002 assessment estimated the lifetime cost for each individual with FAS (adjusting for the change in the cost of medical care services, lost productivity, and inflation) at $2 million. This figure consists of $1.6 million for medical treatment, special education, and residential care for persons with mental retardation, and $0.4 million for productivity losses.28
Where human studies fall short, animal studies can help elucidate causation
Unquestionably, there are flaws in the existing literature on the causation of FAS. Many studies rely on self-reporting by pregnant women, and underreporting in these cases is a real concern. There often are other confounders potentially negatively affecting fetal development, making it difficult to differentiate causation. The animal studies that don’t share these limitations do suggest a causal relationship between antenatal alcohol exposure and poor obstetric outcomes, however.29 These studies suggest mechanisms such as altered gene expression, oxidative stress, and apoptosis (programmed cell death).30
Warren, Hewitt, and Thomas describe how intrauterine alcohol exposure interferes with the function of L1CAM, the L1 cell-adhesion molecule.31 They noted that just one drink could interfere with the ability of L1CAM to mediate cell adhesion and axonal growth. Prenatal alcohol exposure is also thought to contribute to interference in neurotransmitter and N-methyl-D-aspartate receptor coupling, which may have potential therapeutic implications.32
Considerations in FAS identification and treatment
There is a potential to identify alcohol exposure in the womb. The majority of ingested alcohol is eventually converted to carbon dioxide and water in both maternal and fetal circulations, which has hampered the identification of biomarkers for clinical use in FAS. Fatty acid ethyl esters (FAEEs), nonoxidative metabolites of ethanol, may prove to be such markers.33 FAEEs have been measured in a variety of tissues, including blood and meconium. FAEEs can be measured in both neonatal and maternal hair samples.
A study evaluating the utility of such testing in 324 at-risk pregnancies revealed 90% sensitivity and 90% specificity for identifying “excessive drinking” using a cutoff of 0.5 ng/mg.34
Research shows potential therapeutic approaches during pregnancy. While the use of biomarkers has the potential to assist with the identification of at-risk newborns, it merely identifies past alcohol use; it doesn’t necessarily permit identification and prevention of the known negative pediatric sequelae. Preliminary animal studies reveal the potential benefit of neuroprotective peptides to prevent brain damage in alcohol-exposed mice.35 Further research is ongoing.
Treatment: The earlier the better
Early diagnosis and a positive environment improve outcomes. It is well established that early intervention improves outcomes. One comprehensive review of 415 patients with FAS noted troubling outcomes in general for adolescents and adults.36 Over their life spans, the prevalence of such outcomes was:
- 61% for disrupted school experiences
- 60% for trouble with the law
- 50% for confinement (in detention, jail, prison, or a psychiatric or alcohol/drug inpatient setting)
- 49% for inappropriate sexual behaviors on repeated occasions
- 35% for alcohol/drug problems.
The odds of escaping these adverse life outcomes are increased up to fourfold when the individual receives a FAS or FASD diagnosis at an earlier age and is reared in a stable environment.36