Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD). Fetal Alcohol Syndrome (FAS) is part of this group and was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities and defects of the central nervous system (CNS). The CNS is particularly vulnerable to the effects of ethanol during prenatal development. Severe exposure correlates with gross morphological abnormalities and an overall decrease in white matter. Mechanisms for how ethanol affects the development of the CNS are complicated, but damage to neural stem cell progenitor pools that give rise to neurons and glia is strongly suspected to be a major factor. Damage to this population of cells at any point during CNS development can result in abnormalities in the formation and maturation of these cells, from the initial differentiation through the maturation of neuronal networks. This damage can lead to a wide variety of cognitive deficiencies, functional impairments, and behavioral problems depending on the area of the brain impacted by prenatal ethanol exposure.

The term Fetal Alcohol Syndrome (FAS) was first published in 1973 in an article published in the British medical journal The Lancet. In that article, a group of pediatricians and psychiatrists at the University of Washington Medical School helped to define the morphological defects and developmental delays that can affect children born to alcoholic mothers. Those observations include pre- and post-natal growth deficiencies, minor facial abnormalities, and damage to the developing brain that can result in behavioral, learning, and cognitive abnormalities.

In the US, one in 1000 births is affected by neural tube defects (NTD). A neural tube defect is a birth defect involving the malformation of body features associated with the brain and spinal cord. An NTD originates from and is characterized by incomplete closure of the neural tube, which is an organizer and precursor of the central nervous system. In humans, incomplete closure of the neural tube during embryonic development results in anatomical abnormalities such as anencephaly (a severe lack of skull and brain), hydranencephaly (cerebral hemispheres replaced with sacs of cerebrospinal fluid), spina bifida occulta (incompletely closed lower spinal cord), iniencephaly (severe retroflexed head and spinal defects), and encephalocele (a sac-like protrusion from an opening somewhere along the midline of the skull).

Maternal consumption of alcohol (ethanol) can result in a range of alcohol-induced developmental defects. In humans, those collective birth defects are called Fetal Alcohol Spectrum Disorders, with the most severe manifestation being Fetal Alcohol Syndrome (FAS). FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). The eye and ocular system development is particularly susceptible to the effects of prenatal alcohol exposure and can result in visual impairment or blindness.

Parasitic twins, a specific type of conjoined twins, occurs when one twin ceases development during gestation and becomes vestigial to the fully formed dominant twin, called the autositic twin. The underdeveloped twin is called parasitic because it is only partially formed, is not functional, or is wholly dependent on the autositic twin. In most cases, the phenotype of parasitic twins is one normal functioning individual with extra appendages or organs, leading to questions about whether or not the additional limbs and organs are in fact another person or just a mutation of the individual's body. Researchers think that parasitic twins result from mechanisms similar to those that produce Vanishing Twin Syndrome. On a developmental continuum with vanishing twin syndrome on one end and developmentally normal twins on the other, researchers propose that the patterns of conjoined twins fall in the middle.

Prenatal exposure to alcohol (ethanol) in human and animal models results in a range of alcohol-induced developmental defects. In humans, those collective birth defects are called Fetal Alcohol Spectrum Disorders, with the most severe manifestation being Fetal Alcohol Syndrome (FAS). FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). The basal ganglia, one of the central nervous system components, are affected by exposure to ethanol during development. When exposed to alcohol in utero, the basal ganglia decrease in size resulting in poor motor coordination and defects in executive functioning.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading fetal alcohol spectrum disorders (FASD). Fetal alcohol syndrome (FAS) is the most severe combination of these defects under this heading, and is characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system (CNS). The developing brain is particularly vulnerable to the toxicity of ethanol, given the broad time frame of susceptibility from neurulation, when the neural tube is formed, all the way through to birth. The cerebellum is an area of the brain particularly vulnerable to prenatal ethanol exposure. Mechanisms proposed for this drastic reduction in brain cells include apoptosis, oxidative stress, and damage to the radial glia stem cell progenitor pool. Physical dexterity, coordination, and visuospatial processing are all affected by these stressors, and eyeblink classical conditioning tests have proven that ethanol-induced damage goes beyond motor coordination by permanently impacting learning and memory.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD). Fetal Alcohol Syndrome (FAS) was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system. The pattern of facial defects that occur as a result of ethanol exposure during development primarily affects the midline of the face, altering morphology of the eyes, nose, and lips. Ethanol damage to cranial neural crest cells (CNCC) early in embryonic development is responsible for these minor midline abnormalities. Regulation of the gene sonic hedgehog (shh) during this period of development has been observed to rescue these ethanol-affected CNCC from fated cell death, an association that has not yet been examined as it applies to human cells.

Cystic fibrosis (CF) is a fatal, inherited disease found in humans and characterized by buildup of thick, sticky mucus, particularly in the respiratory and digestive tracts. The abnormally thick mucus prevents the pancreas from functioning normally; it often leads to digestive problems and chronic lung infections. Cystic fibrosis is most prevalent in Caucasian individuals, and approximately 1 in every 29 individuals in the US is a carrier for the mutated CF gene. There are an estimated 30,000 reported cystic fibrosis cases in the US, and 70,000 reported cases worldwide, although the international number is undoubtedly low due to underreporting or early deaths.

Estrogen plays a key role in the regulation of gene transcription. This is accomplished by its ability to act as a ligand and to bind to specific estrogen receptor (ER) molecules, such as ERα and ERβ, which act as nuclear transcription factors. There are three major nuclear estrogen receptor protein domains: the estrogen binding domain, the protein interaction domain, and the DNA binding domain. The domain responsible for the regulation of transcription is the DNA binding domain, which binds to DNA sequences called estrogen-responsive elements (EREs), found in enhancer regions of specific genes. By the binding of estrogen or an estrogen mimic to these enhancers, the target genes become activated and the proteins produced are involved in numerous cellular processes. With an estrogen mimic or xenoestrogen, such as diethylstilbestrol (DES), the negative regulation of certain genes during embryonic development can be devastating to the developing anatomy, especially the reproductive system.