Abstract
The magnitude of the detrimental effects following in utero alcohol exposure, including fetal alcohol syndrome and other fetal alcohol spectrum disorders (FASD), is globally underestimated. The effects include irreversible cognitive and behavioral disabilities as a result of abnormal brain development, pre- and postnatal growth retardation and facial dysmorphism. Parental alcohol exposure and its effect on offspring has been recognized for centuries, but only recently have we begun to gain molecular insight into the mechanisms involved in alcohol teratogenesis. Genetic attributes (susceptibility and protective alleles) of the mother and the fetus contribute to the risk of developing FASD and specific additional environmental conditions, including malnutrition, have an important role. The severity of FASD depends on the level of alcohol exposure, the developmental stage at which exposure occurs and the nature of the exposure (chronic or acute), and although the most vulnerable period is during the first trimester, damage can occur throughout gestation. Preconception alcohol exposure can also have a detrimental effect on the offspring. Several developmental pathways are affected in FASD, including nervous system development, growth and remodeling of tissues, as well as metabolic pathways that regulate glucocorticoid signaling and balanced levels of retinol, insulin and nitric oxide. A body of knowledge has accumulated to support the role of environmentally induced epigenetic remodeling during gametogenesis and after conception as a key mechanism for the teratogenic effects of FASD that persist into adulthood. Transgenerational effects are likely to contribute to the global burden of alcohol-related disease. FASD results in lifelong disability and preventative programs should include both maternal alcohol abstention and preconception alcohol avoidance.
Highlights
The magnitude of the detrimental e ects following in utero alcohol exposure, including fetal alcohol syndrome and other fetal alcohol spectrum disorders (FASD), is globally underestimated
It is possible that many idiopathic neurodevelopmental disorders, including some cases of autism and attention deficit hyperactivity disorder (ADHD), may be attributable to transgenerational effects of alcohol exposure
In the USA, it is estimated that FASD may affect up to 1% of the population [10] and incur considerable costs [11], but the prevalence, especially in middle to low income countries, may be considerably higher than reported estimates [12,13]
Summary
The magnitude of the detrimental e ects following in utero alcohol exposure, including fetal alcohol syndrome and other fetal alcohol spectrum disorders (FASD), is globally underestimated. Many animal studies have shown that clinical severity following in utero ethanol exposure correlates with the developmental stage (timing), the dose and the frequency of exposure (chronic versus acute) [16,17]; it is the result of complex gene-environment interactions that alter gene expression patterns, especially during development. Rodent models have been used most often (especially the mouse and rat) and various regimens of alcohol administration have resulted in remarkable phenotypic similarities with the features of FASD in humans, including distinctive craniofacial alterations, stunted growth and behavioral abnormalities.
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