Thus, PAE after major organogenesis may result in a FASD phenotype with neurodevelopmental disorder but without physical alterations, making diagnosis difficult80. Nutritional deficiency during pregnancy may potentiate the effects of PAE on developmental outcomes, and maternal alcohol intake may further reduce the availability of developmentally important nutrients87. Fetal alcohol spectrum disorders (FASDs) are a group of conditions that can occur in a person exposed to alcohol before birth. These conditions can affect each person in different ways and can range from mild to severe. People with FASDs can have lifelong effects, including problems with behavior and learning as well as physical problems. Fetal alcohol syndrome is on the severe end of fetal alcohol spectrum disorders (FASD).
Although based on clinical consensus, these strategies form the basis for future research256. If you did drink any amount of alcohol during pregnancy, it’s important to know that your healthcare provider and your baby’s pediatrician need to know to help you plan for your child’s future. This condition can be prevented if you don’t drink any alcohol during pregnancy. It’s possible that even small amounts of alcohol consumed during pregnancy can damage your developing fetus.
Myelination of the optic nerve is disrupted in animal models of FASD, with reports of decreased thickness, as well as aberrant and fewer myelin sheaths (Samorajski et al., 1986; Phillips and Krueger, 1992; Parson et al., 1995; Pinazo-Duran et al., 1997). Developmental alcohol exposure interferes with oligodendrocyte maturation and delays expression of MBP resulting in ultrastructural harm to the myelin sheaths and a decreased number of myelinated optic nerve axons (Guerri et al., 2001). Such alterations in myelin may be responsible for the hypoplasia of the optic nerve present in FAS.
Thus, alcohol exposure disrupts the development and maturation of radial glia cells that act both as precursor cells for neurons, astrocytes and oligodendrocytes, as well as aid in the migration of other progenitor cells throughout the developing CNS (Table 2). Fetal Alcohol Syndrome is a condition that develops in a baby exposed to alcohol before birth. A child with fetal alcohol syndrome may have specific abnormal facial features, small head size, and problems with development including delayed language, learning, and poor impulse control. Children with fetal alcohol syndrome are at high risk for problems such as Attention-Deficit/Hyperactivity disorder (ADHD), intellectual disability, learning problems, and emotional issues.
Disruptions in survival and maturation of oligodendrocytes are likely to impair the formation of neurocircuitry and the efficient conduction of neuronal signals. Future studies are needed, however, to elucidate the effects of alcohol on oligodendrocytes and OPCs to understand the pathways that lead to alcohol-induced dysfunction. As previously described, at first glance, prenatal exposure to alcohol may not be expected to exert a substantial effect on myelination in adults, given that much of the myelination that drunken baby syndrome occurs in humans happens long after birth.
Preliminary evidence suggests that web-based or app-based mobile health interventions may mitigate patient stigma and reluctance to report alcohol use and might circumvent barriers related to clinician time constraints, training and motivation209. Similarly, mobile health approaches may reduce alcohol and substance use in the preconception, prenatal, and postnatal periods209 and improve access to interventions for families in rural and remote settings. Empathic, compassionate support of abstinence during pregnancy may improve opportunities for treatment of substance use disorders22,47,196,202. Screening for alcohol and substance use should be repeated throughout pregnancy and equally across populations to avoid stigmatizing marginalized populations with selective screening22,196,210,211. People who screen positive should be directed to a well-developed management pathway for clinical care. Early identification of FASD is critical for the well-being of individuals affected by prenatal alcohol exposure and their families.
This study also observed a greater percentage of cells derived from alcohol-exposed embryos remaining as radial glia in culture as opposed to differentiating into neurons or astrocytes following 2 days of culture compared to control cultures (Rubert et al., 2006). Alcohol exposure damages neural progenitor cells, limiting their survival and impeding their differentiation into astrocytes (Taléns-Visconti et al., 2011; Nash et al., 2012). Culture models using neurospheres also demonstrate that selective exposure of neural precursor cells to alcohol impairs cell division and astrocyte formation (Vemuri and Chetty, 2005).