Alcohol and Pregnancy Science


Alcohol and Pregnancy Science
Alcohol, like the chemical element mercury, is a confirmed teratogen (a substance that interferes with normal prenatal development). Alcohol can cause central nervous system (brain and spinal cord) malformations with associated neurobehavioral dysfunction. By comparison, lead is a neurotoxin but not a teratogen in that it produces neurobehavioral dysfunction in the absence of brain and spinal cord malformations.

Science definitively recognizes that when a pregnant woman consumes alcohol, the alcohol crosses the placenta into the blood supply of the developing embryo or fetus. An embryo or fetus has neither the developed organ systems nor enzymes able to metabolize alcohol.

The first paper in the medical literature describing a constellation of birth defects linked to prenatal alcohol exposure was published in France in 1968 by Dr. Paul Lemoine.

The first paper in U.S. medical literature appeared in 1973 authored by Drs. David Smith and Ken Lyons Jones. As of 2012, nearly 4,000 papers have been published confirming the toxicity of alcohol to the embryo or fetus, the underlying mechanisms of alcohol-induced damage to the embryo or fetus, and the physical and functional birth defects related to prenatal alcohol exposure.

No published study has suggested that alcohol is not a teratogen or demonstrated that prenatal alcohol use has any potential benefit to human development.

As described by the Institute of Medicine, the basic and biomedical research demonstrates that alcohol damages the developing brain through multiple actions at different cellular sites interfering with normal development by disrupting cell migration, cell functions, and causing cell death.

Alcohol can cause damage to multiple regions of the brain, specifically to the corpus collosum (connects brain hemispheres), cerebellum (consciousness and voluntary processes), basal ganglia (movement and cognition), hippocampus (emotional behavior and memory), hypothalamus (sensory input), among other neural regions.

Ethanol is the principal psychoactive constituent in alcoholic beverages. In utero it has been found to:

  • Interfere with normal proliferation of nerve cells;
  • Increase the formation of free radicals–cell damaging molecular fragments;
  • Alter cells ability to regulate cell growth, division and survival;
  • Impair the development and function of astocytes, cells that guide the migration of nerve cells to their proper places;
  • Interfere with the normal adhesion of cells to one another;
  • Alter the formation of axons, nerve cell extensions that conduct impulses away from the cell body;
  • Alter the pathways of biochemical or electrical signals within cells;
  • Alter the expression of genes, including genes that regulate cell development.

Human development occurs in an orderly process of biochemical and structural transition during which new constituents are being formed and spatially arranged throughout gestation. At any time in the span of development these ongoing processes can be subtly or severely disturbed or abruptly halted resulting in abnormal development or fetal death.

Therefore, at any time alcohol is present it has the potential to harm development. For example, the hallmark facial dysmorphology associated with Fetal Alcohol Syndrome will only occur if alcohol is present during the specific window of development.

Of all the substances of abuse, including marijuana, cocaine and heroin, alcohol produces by far the most serious neurobehavioral effects on the embryo or fetus.

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