Many pregnant women are not aware of the complications that are involved with pregnancy. Majority of young women look at 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 also to the fetus that she is carrying. The problem is FAS, Fetal Alcohol Syndrome. According to many physicians it is the leading cause of birth defects and developmental disabilities in the United States today. Douglas A. Milligan states that, “FAS is the single greatest cause of mental retardation in the U.S. today” (Seachrist, p. 314). Fetal Alcohol Syndrome was first named and treated and found in the late 1960’s. This condition 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. FAS consists of a characteristic pattern of abnormalities resulting from the exposure that the fetus has had with alcohol during early development. There have been many reports linking alcohol use and fetal deficiencies in growth that emerged from France in the late 1950’s. Not until the 1960’s was the correlation made between the number of defects and the increasing amount of babies born with the syndrome. 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. Being further studied in the 1970’s under the heading as a birth defect that occurs, FAS was one of the most common causes of birth defects.
Researchers said that it occurred in almost 1 of every 500 to 1 in every thousand births ( Seachrist, p. 314). There is a major thing that causes difficulty in the diagnosis of this disorder though, its main diagnosis hinges on the obvious facial abnormalities, short stature, and low IQ. Children who do not meet all of these factors are diagnosed with FAE, Fetal Alcohol Effect, a milder form of FAS. 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. As I stated before many factors do play a role in the development of FAS in an infant. The most prominent among these are the frequency and the quantity of maternal alcohol consumption during the pregnancy. The timing of the 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 FAS. There are specifics in diagnosing that doctors look for in treating a patient for FAS. First of all the eyes are the most common and consistent sign of FAS, 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 (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. Following the downward pattern, the next common facial defect in children of FAS/FAE is slow growth in the center of the face. This produces an underdeveloped mid-face 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 tends to point forward and downward in that same respect (Aase, p.5).
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 “cupid’s bow”. In the development of the FAS 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, p.5). Looking inwardly to the problems that may occur children with FAS 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 aforementioned abnormalities are not specific to FAS but coupled with FAS characteristics they help to provide a more clear and concise diagnosis. There were many reports of behavioral and intellectual trouble in all the children that have thus been diagnosed. Beginning with infancy, the children have problems at feeding and are highly irritable. They also exhibit unpredictable sleeping and eating patterns that make it hard for the baby to be cared for and for maternal bonding to occur. During development, both physical and mental, FAS children have very fine and poor motor coordination skills and it becomes very apparent at the preschool age. They also are 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 (ADHD); 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 FAS children grow into FAS 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 FAS.
The two things involved that stand out the most are teratogens and acetaldehydes. These two stand out as the things that are not in a detailed way nutritionally involved. No laboratory tests can rule out the diagnosis of FAS but growing research is directed toward finding the underlying mechanisms that contribute to fetal alcohol damage. Scientists also are searching for genetic and biochemical characteristics associated with the susceptibility to FAS. “Human gestation is divided into two major periods: the embryonic period (up to 8 weeks) and the fetal period (from 8 weeks to delivery). It’s 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” (Michaelis and Michaelis, p. 17). The primary metabolic product of alcohol is acetaldehyde, which could also produce some damaging effects. The reasons that this is looked at, but not as directly as is alcohol, is because, alcohol is distributed rapidly and nearly equally in maternal and fetal tissues. Also when alcohol is applied directly onto embryos in vitro conditions in which no acetaldehyde is formed, it causes growth retardation. Because of this, these two mentioned factors are in effect causes indirectly, if not adversely directly, to the formation of the defects that are causes in the children of FAS. The nutritional aspect of FAS is not as simple. Normal growth and development during this priming 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, through research with rat embryos, have proven that the depravity of such causes malformations of fetal tissue’s energy sources. The materials needed for cell proliferation, growth, and differentiations are also affected in this. The supplemental glucose thus becomes only minimally effective because of the lack of diminution of fetal growth retardation (Michaelis and Michaelis, p. 21). Included within the nutritional deficiencies that occur are the loss of vitamins B6 and A.
There 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 it functions as protein metabolism. There exists also a possible defect in the metabolism of folic acid. The lack of which during the gestation period produces malformations in the fetus. Vitamin A deficiency revolves around the receiving of vitamin A from the alcoholic mother to the fetus via the placenta. There is no sufficient 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 nutritionally diet of the mother. Retinoic acid functions as a chemical agent of the activation of DNA. The lessening of this particular vitamin is responsible for the delays and malformations seen in FAS (Michaelis and Michaelis, p. 22).
The release and production of hormonal factors are needed to be supplied to the fetus through the mother for normal development and this is yet 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. In experimental animals exposed in the uterus to alcohol, there is a decrease in blood and brain concentration of the corticosteroid hormones. The deficiency in hormone leads to the failure in the response of a newborn to stress. Thyroid hormonal deficiencies are also harmful effects on the development of some tissues, especially the brain. In the cerebellum, a part of the brain controlling posture and balance, there is a change in the maturation and migration of nerve cells to their respective locations that is caused by the deficiencies linked to the thyroid hormone (Michaelis and Michaelis, P. 19).
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. The increased production and release of the substances that are produced by the prostaglandin and its developmental hypoxia can diminish blood circulation to tissues and set the stage for the cessation or delay in cell proliferation, growth, and migration (Michaelis and Michaelis, p. 16).
There are many things that are factors in the growth and continual deformation in the babies born with FAS 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 FAS. There will always exist a continual risk because of the lack of education in mothers-to-be.
The one thing most importantly stressed is that a mother who knows or even thinks that she is pregnant should not drink anything that is made of alcohol. Educating these mothers of the harm that they can cause themselves and their unborn children is what we needs to be done. 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.
1.Aase, Jon M. Clinical Recognition of FAS: Difficulties of Detection and Diagnosis. Alcohol Health and Research World, Vol. 18, No. 1, Pgs 4-6, Winter 1994. 2. Michaelis, Elias and Michaelis, Mary L. Cellular and Molecular Bases of Alcohol’s Terato genic Effects. Alcohol Health And Research World, Vol. 18, No. 1, Pgs 11-26, Winter 1994. 3.Prenatal Alcohol Exposure and Psychomotor Development. American Family Physician, Vol. 53, No. 8, Pgs 26-40, June 1996. 4. Seachrist, Lisa. Birth Defects Too Often Blamed On Alcohol. Science News, Vol. 148, No. 20, Pg.314, November 1995.