Fetal alcohol spectrum disorders and their transmission through genetic and epigenetic mechanisms

Edward A. Mead, Dipak K. Sarkar

Research output: Contribution to journalReview articlepeer-review

75 Scopus citations

Abstract

Fetal alcohol spectrum disorders (FASD) are a group of related conditions that arise from prenatal exposure to maternal consumption of the teratogen, ethanol. It has been estimated that roughly 1% of children in the US suffer from FASD (Sampson et al., 1997), though in some world populations, such as inhabitants of some poorer regions of South Africa, the rate can climb to as high as 20% (May et al., 2013). FASD are the largest cause of mental retardation in U.S. neonates, and ironically, are entirely preventable. FASD have been linked to major changes in the hypothalamic-pituitary-adrenal (HPA) axis, resulting in lifelong impairments through mental disorders, retardation, and sensitivity to stress. FASD are linked to an impaired immune system which consequently leads to an elevated risk of cancer and other diseases. FASD arise from a complex interplay of genetic and epigenetic factors. Here, we review current literature on the topic to tease apart what is known in these areas particularly emphasizing HPA axis dysfunction and how this ties into new studies of transgenerational inheritance in FASD.

Original languageEnglish
Article numberArticle 154
JournalFrontiers in Genetics
Volume5
Issue numberJUN
DOIs
StatePublished - 2014
Externally publishedYes

Keywords

  • FASD
  • Fetal alcohol
  • HPA axis
  • Proopiomelanocortin
  • Transgenerational epigenetic

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