Fetal Alcohol Syndrome Essay

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According to the U.S. Census Bureau 10,657 babies are born every day and twenty of these babies are born with Fetal Alcohol Syndrome.  Alcohol is the most commonly abused substance by pregnant women because it legal and socially acceptable (Mercer, 1990).  Many pregnant women are not aware of the complications that are involved with pregnancy.  A greater majority of young women see pregnancy as a way of bringing a life into the world but do not use precaution in their dietary habits to prevent the destruction or inhibition of such a life. Most pregnant women continue on their drinking and drug abuse binge right throughout their pregnancy.  They do not think ahead to the inexplicable damage that it could do to their fetus.  What they do not know is that when a woman drinks while pregnant it could do damage, and pose problems not only to herself, but to the fetus that she is carrying.  When alcohol is combined with pregnancy it can cause devastating effects in the fetus (Seachrist, 1995).

Fetal alcohol syndrome is characterized by structural abnormalities of the head and face including microcephaly, flattening of the maxillary area, intrauterine growth retardation, decreased birth weight and length, developmental delays, intellectual impairment, hyperactivity, altered sleep pattern, feeding problems, perceptual problems, impaired concentration, mood problems, and language dysfunction.  Fetal alcohol syndrome is the number one cause of mental retardation in the United States and is one hundred percent preventable (Olson, 1994).  It is a national health problem that was first identified, treated, and found in the late 1960s.  The term fetal alcohol syndrome was coined to describe the pattern of the abnormalities found in some children born to alcoholic women.

It clearly was very noticeable and distinctive in the recognition of itself and was distinct from all other patterns of malformation in the fetus; there was a significant association found between the alcohol consumption rates during pregnancy and a lower general cognitive index of these children (Seachrist, 1995).  Alcohol use during pregnancy also increases the risk for abruptio placentae, stillbirth, spontaneous abortion, congenital anomalies, prematurity, postmaturity, and infections (Cook, et al., 1990).

The effects of fetal alcohol syndrome are not always so drastic, some children are born with less dramatic physical defects.  Often though, many people with this may look quite normal but may have significant deficits. Such deficits as intellectual, behavioral, and social behaviors.  Fetal alcohol syndrome may be difficult to diagnose, because its main diagnosis hinges on the obvious facial abnormalities, short stature, and low IQ. Children that do not meet all of these factors are diagnosed with fetal alcohol effect (Aase, 1994).  Fetal alcohol effect is a syndrome in which children suffer some but not all of the symptoms of fetal alcohol syndrome.  It occurs in children whose mothers have used varying amounts of alcohol while pregnant, including those who engaged only in occasional binge drinking.  Fetal alcohol effects are seen three more times more often than fetal alcohol syndrome (Robertson, 1993).

There are general abnormalities that affect both forms of the disease.  These abnormalities include a deficiency in growth, a pattern of malformation affecting the face, heart, and urinary tract.  There are abnormalities within the brain that lead to various intellectual and behavioral problems in early childhood, as well as problems within the central nervous system.  The timing of gestation of alcohol is what determines the level of abnormalities that occur.  The stage of development at which alcohol consumption takes place and that in correlation to the gestation period, nutritional status, and genetic background all play parts in the development of the baby and its defects.  The alcohol that is being consumed does have an effect on the cellular and molecular development of the fetus and that is what generally underlies the development of fetal alcohol syndrome.

There are specifics in diagnosing that doctors look for in treating a patient with fetal alcohol syndrome.  First of all the eyes are the most common and consistent sign of fetal alcohol syndrome, the eyelids especially. Children often appear to have widely spaced eyes but measurements reveal that they are spaced apart normally. This disparity in sight is caused by short fissures or eye openings. The distance between the inner and outer corners of each eye is palpebral shortened making the eyes appear smaller and farther apart than normal. The next common facial defect in both fetal alcohol syndrome and fetal alcohol effect is slow growth in the center of the face.  This produces an underdeveloped midface and the zone between the eye and the mouth may seem to be flattened or depressed and in congruence the bridge of the nose is often very low.  As a result of slow nose growth, the nose tend to point forward and downward in the same manner.  Subtle but still a characteristic feature is the philtrum, the area between the nose and the mouth.

Characterized by a vertical midline groove, bordered by two vertical ridges of the skin, where the grooves meet the red margin of the upper lip it forms a cupids bow.  In the development of the fetal alcohol syndrome child there is a long, smooth philtrum without the ridges that should be there coupled with a smoothly arched upper lip margin.  Where as the facial abnormalities are very obvious when looked for the abnormalities of the limbs and joints are less consistent.  These include deformities of the small joints of the hands as well as an incomplete rotation at the elbow (Aase, 1994).  Looking inwardly to the problems that may occur children with fetal alcohol syndrome are also for the most part stricken with an increased risk for many common birth defects.

Of these chronic defects include congenial heart disease, abnormalities of the urinary tract and genitals, and spina bifida.  These abnormalities are not specific to fetal alcohol syndrome but are coupled with fetal alcohol characteristics and help to provide a more clear and concise diagnosis.  There were many reports of behavioral and intellectual trouble in all the children that have been diagnosed.  Beginning with infancy, the children have problems at feeding and are highly irritable.  They also exhibit unpredictable sleeping and eating patterns, which make it hard for the baby to be cared for and for maternal bonding to occur.  During development, both physical and mental, these children have very fine and poor motor coordination skills and it becomes very apparent at the preschool age.  They are also very affectionate, but at the same time very hyperactive which makes it a problem for the teachers who have them in class to deal with.

This is why they are, during the first few years of school, given the diagnosis of having attention-deficit hyperactivity disorder.  This diagnosis is given because of their high activity level, short attention span, and poor short-term memory.  Many of these children require special education help regardless of the fact that their IQ falls between the normal range.  Their hyperactivity calls for them to receive special attention that normal teachers cannot and at most time will not give them.  As they grow into adults their level of development and how they developed begins to show in everything that they do.  Since their social and mental health has been compromised as adults they exhibit inadequate communication skills, impulsivity, poor judgment, trouble with abstract thinking, and limited problem solving skills.

With all these problems they often have difficulty in holding down a job because of their unreliability, lack of social skills, and functional illiteracy.  There are many different factors involved in fetal development in relation to fetal alcohol syndrome.  The two things involved that stand out are teratogens and acetaldehydes.  These two stand out as the things that are not in a detailed way nutritionally involved.  No laboratory test can rule out the diagnosis of fetal alcohol syndrome but growing research is directed toward finding the underlying mechanisms that contribute to the fetal alcohol damage.  Scientists are also searching for genetic and biochemical characteristics associated with the susceptibility to fetal alcohol syndrome.  Human gestation is divided into two major periods; which is the embryonic period (conception to 8 weeks) and the fetal period (from 8 weeks to delivery).

Its during the embryonic period that various drugs are introduced directly into the maternal bloodstream or administered through the maternal diet.  Chemical/Physical agents that produce these fetal malformations are called teratogens.  Most teratogens show selectivity towards certain organs, based on the timing of the embryo to the teratogen, the dosage taken, and the sensitivity of the dividing cells.  Organs and limbs of the developing embryo are formed from collections of specialized cells.  Exposure of an embryo to a teratogen during this period may have devastating effect on the formation of that organ.

The primary metabolic product of alcohol is acetaldehyde which could also produces some damaging effects. The reason why this is looked at, but not as directly as is alcohol, is because of the following reasons; alcohol is distributed rapidly and nearly equally in maternal and fetal tissue, alcohol applied directly onto embryos in vitro conditions in which no acetaldehyde is formed causes growth retardation.  Because of this, these two mentioned factors are in effect causes indirectly to the formation of the defects that are causes in the children of fetal alcohol syndrome.   (Michaelis & Michaelis, 1994).

The nutritional aspect of fetal alcohol syndrome is not very simple.  Normal growth and development during this period requires the transfer of a continuous supply of amino acids and glucose from mother to fetus.  Several studies have shown that with the human placental tissue alcohol directly obstructs the transport of both these substances.  These are two essential substances that have proven that the depravity of such causes malformations of fetal tissues energy sources.  The materials needed for cell proliferation, growth, and differentiation are also affected in this.  The supplemental glucose therefore becomes only minimally effective because of the lack of diminution of fetal growth retardation.  Included in the nutritional deficiencies that occur are the loss of vitamins B6 and vitamin A.

Еhere is noted decrease in the transfer of B6 from an alcoholic mother to her fetus through the placenta.  This vitamin is especially important in the development of the fetus because if functions as protein metabolism. There exists also a possible defect in the metabolism of folic acid.  If there is a lack of folic acid during the gestation period then malformations in the fetus with be produced.  There is not enough evidence to support that there is actually a vitamin A deficiency, but it appears that the vitamin accumulates in the liver of the alcohol-exposed fetus.  This suggests that the vitamin is not being metabolized normally.  Since this vitamin is supposed to normally produce retinoic acid, which is significant to development, it is a very vital ingredient in the nutritional diet of the expectant mother.

Retinoic acid functions as a chemical agent of the activation of DNA; the lessening of this particular vitamin is said what may be responsible for the delays and malformations seen in fetal alcohol syndrome.  The release and production of hormonal factors are needed to be supplied to the fetus through the mother for normal development and this is another fact that is tampered within the mother who drinks throughout her pregnancy.  The production and release of hormones from both the maternal and fetal glands and from the placenta influence the formation and development of tissues as diverse as the brain and the palate.  Prostaglandins are local tissue chemicals derived from fatty substances.

There is a marked increase in the activity of these chemicals during the exposure that the fetus has to alcohol.  These chemicals have very powerful affects on the blood vessels of the uterus, placenta, and the fetus.  Their overproduction may be responsible for the lack of oxygen brought about by prostaglandin-induced constriction of the blood vessels.  This lack of oxygen functions as a trigger for the cells in different tissues.  This in turn leads to the aggravation of the preexisting hypoxia and could lead to tissue damage and growth retardation. T he increased production and release of the substances that are produced by the prostaglandin and its developmental hypoxia can diminish blood circulation to tissue and set the stage for the cessation or delay in cell proliferation, growth, and migration (Michaelis & Michaelis, 1994).

Fetal alcohol syndrome results from the toxic effect of alcohol and its chemical factors on the developing fetus and its brain.  The alcohol enters the bloodstream through the placenta and then the damage begins to occur. Fetal alcohol syndrome consists of a characteristic pattern of abnormalities resulting from the exposure that the fetus has had with alcohol during early development (Seachrist, 1995).  Moreover, a babies tiny developing system is not equipped to handle alcohol and is effected much more severely than the mother.  No one really knows how much alcohol it takes to harm an unborn baby.  As the consumption increases so do the risks.  One report suggested that not only does alcohol cause birth defects, but it can also create leukemia.  This study included six hundred eleven children younger than eighteen months old, two hundred fifty had leukemia (http://www.babyzone.com/drugs.htm).

Drinking early in pregnancy even before the woman knows she is pregnant increases the chance of having a baby with growth deficiency or birth defects.  Forty four percent of women who drink heavily during pregnancy will have a child with Fetal Alcohol Syndrome.  The other fifty six percent will have effects such as minor learning and behavioral difficulties


There are many things that are factors in the growth and continual deformation in babies born with fetal alcohol syndrome, but there can be many or one simple thing that can also avoid the fetus to be affected by the exposure to alcohol.  There continues to be ongoing research on the nutritional, hormonal, and cellular events regulating fetal development to help guide early interventions in children with fetal alcohol syndrome.  There will always exist a continual risk because of the lack of education in mothers-to-be.  The one thing that needs to be stressed is for a woman is even if she suspects herself to be pregnant she should not drink anything that is made of alcohol.

The educating of these mothers to the harm that they can cause themselves and their unborn children is what we need to focus on and do.  They should know that with the imbalance of their meals and alcohol consumption that their children are suffering and cannot at times be given that chance to live and survive in society as normal children should.  Because of the lack of education that they have they do not understand that what they do to themselves is also what they do to their children.



Cook, P.S., Peterson, R.C., & Moore, D.T. (1990).  Alcohol, tobacco, and other drugs may harm the unborn.  Rockville, MD: U.S. Department of Health and Human Services.

Mercer, R.T. (1990).  Parents at risk.  New York:  Springer, 128

Olson, H.C. (1994).  The effects of prenatal alcohol exposure on child development.  Infants and young children, 6(3), 10-25.

Robertson, B.E. (1993).  Alcohol disabilities primer:  A guide to psychosocial disabilities caused by alcohol use.  Boca Raton:  CRC Press, Inc.


Seachrist, Lisa. Birth Defects Too Often Blamed on Alcohol.  Science News, Nov 1995. v148. n20, p.314(4).

Aase, Jon M. Clinical Recognition of FAS:  difficulties of detection and diagnosis.  Alcohol Health and Research World, Wntr 1994. v18. n1, p.5-10(2).

Michaelis, E. & Michaelis, M.L.  Cellular and Molecular Bases of Alcohols Terato genic Effects.  Alcohol Health and Research World, Wntr 1994.  v18.n1.p.17-22(3).

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