Despite intense research efforts, the exact mechanism for the development of FAS or<unk>  is unknown. On the contrary, clinical and animal studies have identified a broad<unk>  of pathways through which maternal<unk>  can negatively affect the outcome of a pregnancy. Clear conclusions with universal validity are difficult to draw, since different ethnic groups show considerable genetic polymorphism for the hepatic enzymes responsible for ethanol detoxification. Genetic examinations have revealed a continuum of long-lasting molecular effects that are not only timing specific but are also dosage specific; with even moderate amounts being able to cause alterations. A human fetus appears to be at triple risk from maternal<unk>  consumption: # The placenta allows free entry of ethanol and toxic metabolites like acetaldehyde into the<unk>  compartment. The so-called placental barrier is practically absent with respect to ethanol. # The developing<unk>  nervous system appears particularly sensitive to ethanol toxicity. The latter interferes with proliferation, differentiation, neuronal migration, axonic outgrowth, integration, and fine-tuning of the synaptic network. In short, all major processes in the developing central nervous system appear compromised. #<unk>  tissues are quite different from adult tissues in function and purpose. For example, the main detoxicating organ in adults is the liver, whereas the<unk>  liver is incapable of detoxifying ethanol, as the ADH and ALDH enzymes have not yet been brought to expression at this early stage. Up to term,<unk>  tissues do not have significant capacity for the detoxification of ethanol, and the fetus remains exposed to ethanol in the amniotic fluid for periods far longer than the decay time of ethanol in the maternal circulation. The lack of significant quantities of ADH and ALDH means that<unk>  tissues have much lower quantities of antioxidant enzymes, like SOD, glutathione transferases, and glutathion peroxidases, resulting in antioxidant protection being much less effective. Additionally, ethanol may alter<unk>  development by interfering with retinoic acid signaling. Acetaldehyde, the main ethanol metabolite, can compete with retinaldehyde and prevent its oxidation to retinoic acid.
Fetal alcohol spectrum disorder
Attention deficit hyperactivity disorder
Fetal hydantoin syndrome
Williams syndrome
Congenital rubella syndrome
Neonatal encephalopathy
Fetal trimethadione syndrome
Fetal warfarin syndrome