Fetal Alcohol Growth Restriction and Cognitive Impairment

Abstract

BACKGROUND: Although both fetal and long-term growth restriction are well documented in fetal alcohol spectrum disorders, effects on pattern of growth trajectory have not been characterized. Furthermore, the degree to which growth trajectories are related to fetal alcohol-related neurocognitive deficits is unknown.

Relationships of maternal body mass index and plasma biomarkers with childhood body mass index and adiposity at 6 years: The Children of SCOPE study

“…We found an inverse association between maternal alcohol use in the first trimester and BFP at age 6 years following adjustment for confounders. Heavy alcohol exposure during early life or prepregnancy is associated with reduced birthweight and adverse pregnancy outcomes, which may have a persistent influence on childhood growth. A recent study of over 7000 British mother‐child dyads (ALSPAC birth cohort) demonstrated a similar association in young children; however, this was no longer evident at the age of 10 years .…”

Fetal alcohol spectrum disorder predisposes to metabolic abnormalities in adulthood

“…Immediately following EAE, AB strain larvae displayed mild growth restriction, consistent with the short stature phenotypes typical of human FAS (Supplemental Figure 2, A-C, and ref. 34). When removed from ethanol, larvae exhibited compensatory growth and reached the same size as control-matched siblings by 20 dpf (Supplemental Figure 2D).…”

Alcohol‐Related Alterations in Placental Imprinted Gene Expression in Humans Mediate Effects of Prenatal Alcohol Exposure on Postnatal Growth

“…Our prior findings linking growth trajectory pattern to severity of neurocognitive impairment in FASD (Carter et al, 2016a) suggest that deficits in growth and neurobehavior may share common mechanisms. Future studies are needed to determine whether the alcohol-related alterations in gene expression that we have found to be related to somatic growth play a role in fetal alcohol neurobehavioral deficits in humans.…”

“…Three summary measures were constructed by averaging across pregnancy: oz AA/d; oz AA/occasion; and frequency of drinking. We have previously validated this ascertainment protocol in relation to levels of fatty acid ethyl esters in meconium samples in this community (Bearer et al, 2003) and in relation to a broad range of infant (Jacobson et al, 2002) and child outcomes (e.g., Carter et al, 2016a;Jacobson et al, 2008;Lindinger et al, 2016;Meintjes et al, 2014).…”

“…This study has limitations common to other longitudinal studies of prenatal alcohol exposure. Noise surrounding estimates of maternal alcohol consumption may obscure some associations, but differences between true and estimated exposure are likely small, given the validity of the interviewing techniques, which has been demonstrated in relation to meconium levels of fatty acid ethyl ester metabolites of alcohol in this community (Bearer et al, 2003), infant and child behavior (Jacobson et al, 2002(Jacobson et al, , 2008Lindinger et al, 2016), somatic growth (Carter et al, 2016a), and brain structure (De Guio et al, 2014;Fan et al, 2016;Meintjes et al, 2014) and function (Woods et al, 2015). Variability in placental sample collection time may have added variability in RNA detection.…”