Gestational alcohol is an early life stressor that greatly dysregulates the embryonal nervous system structure and functions.
Fetal Alcohol Spectrum Disorders represent a plethora of disruptions leading to neurobehavioral and morphological aberrations.
Gestational alcohol by epigenetic mechanisms may alter the chromatin structure redrawing the gene expression entire pattern.
An early FASD diagnosis using reliable markers of ethanol intake, may offer useful possibilities of intervention.
Supplementing a mother’s diet with protective and antioxidant compounds can protect newborns from being affected.
Ethanol exposure during gestation is an early life stressor that profoundly dysregulates structure and functions of the embryonal nervous system, altering the cognitive and behavioral development. Such dysregulation is also achieved by epigenetic mechanisms, which, altering the chromatin structure, redraw the entire pattern of gene expression. In parallel, an oxidative stress response at the cellular level and a global upregulation of neuroendocrine stress response, regulated by the HPA axis, exist and persist in adulthood.
This neurobehavioral framework matches those observed in other psychiatric diseases such as mood diseases, depression, autism; those early life stressing events, although probably triggered by specific and different epigenetic mechanisms, give rise to largely overlapping neurobehavioral phenotypes.
An early diagnosis of prenatal alcohol exposure, using reliable markers of ethanol intake, together with a deeper understanding of the pathogenic mechanisms, some of them reversible by their nature, can offer a temporal “window” of intervention. Supplementing a mother’s diet with protective and antioxidant substances in addition to supportive psychological therapies can protect newborns from being affected.
The opinions expressed in this post are those of the authors. They do not purport to reflect the opinions or views of the FASD Prevention Conversation Project, its stakeholders, or funders.