Alcohol Consumption During Pregnancy

Abstract

Alcohol is a potent teratogen in humans, and prenatal alcohol exposure is a leading preventable cause of birth defects and developmental disabilities. The term fetal alcohol syndrome (FAS) refers to a pattern of birth defects found in children of mothers who drank during pregnancy. FAS has four criteria: maternal drinking during pregnancy, a characteristic pattern of facial abnormalities, growth retardation, and brain damage (often manifested by intellectual difficulties or behavioral problems). As surveillance and research have progressed, it has become clear that FAS is but a rare example of a wide array of defects that can occur from exposure to alcohol in utero. At least 1 in 10 women will continue to consume alcohol during pregnancy, putting their fetuses at risk for the effects of alcohol exposure.Nurses are in a key position to provide care and conduct research that will contribute to the prevention of the adverse effects of prenatal alcohol exposure during the preconception and perinatal periods, as well as deal with the negative outcomes of exposure in the developing infant. Many areas have yet to be evaluated. Screening tools and interventions have been developed and tested, mostly in majority cultures. Culturally sensitive instruments must be generated and validated for high-risk groups such as Native Americans. Fetal alcohol biomarkers and genetic research are new and need considerably more work. Effective “no drinking during pregnancy” campaigns for high-risk groups must be created and tested. Nurses are well placed to conduct research that will describe the effects at social, behavioral, and biological levels; develop middle-range theories targeted at preventing the drinking behavior and optimizing care of affected children after birth; and generate and test effective interventions that enhance prevention strategies in the 21st century.

Acute and chronic effects of some dietary bioactive compounds on folic acid uptake and on the expression of folic acid transporters by the human trophoblast cell line BeWo

“…First, we investigated the acute and chronic effects of cell exposure to ethanol because this agent is recognized as a potent teratogen in humans [39]. Indeed, prenatal alcohol exposure can give rise to alcohol-related birth defects such as spontaneous abortion, decreased immune function, attention problems, hearing impairment [40] and, as mentioned above, FASD [41].…”

“…Indeed, prenatal alcohol exposure can give rise to alcohol-related birth defects such as spontaneous abortion, decreased immune function, attention problems, hearing impairment [40] and, as mentioned above, FASD [41]. Among children with FASD, a small population presents a specific set of anomalies (specific facial abnormalities, intrauterine growth retardation and significant impairments in neurodevelopment) [39,[42][43][44], known as fetal alcohol syndrome (FAS). FAS is the major known cause of mental retardation in the western world [44] and occurs in 1.9 per 1000 live births [42].…”

Stabilization of IGFBP-1 mRNA by ethanol in hepatoma cells involves the JNK pathway

“…Interestingly, several metabolic and growth effects of elevated IGFBP-1 levels such as fetal growth deficiency and erosion of lean body mass are reminiscent of the toxic consequences observed during chronic alcohol abuse [17,18]. This led to the hypothesis that IGFBP-1 induction during alcohol intoxication could mediate some of the effects of alcohol.…”

Alcohol and thiamine deficiency trigger differential mitochondrial transition pore opening mediating cellular death

“…Alcohol is a potent teratogen in humans, and prenatal alcohol exposure is a leading cause of intrauterine growth retardation and related microencephaly, brain damage often manifested by intellectual disability and behavioral disorders [1,2]. Maternal alcohol use is often concurrent with other factors that pose a risk to the developing fetal brain such as poor nutrition and nutrient factors deficits.…”