Alcohol and Pregnancy, Research Paper Example

Many people are probably surprised to learn that the topic alcohol and pregnancy is not synonymous with fetal alcohol syndrome. There is indeed a difference, and in this brief paper I will touch upon them. But first: is it safe to drink while pregnant? For moderate drinkers, yes.

History

Concern with alcohol and pregnancy may be said to have begun with the Bible. Judges 13:7 warns Behold thou shalt conceive, and bear a son; and now drink no wine nor strong drink. But despite allegedly documented claims to the contrary, there is no evidence that any ancient classical authors from Aristotle onward ever made a connection between alcohol and the symptoms that match today’s fetal alcohol syndrome, known as FAS (Sanders). But well over a century before William Hogarth painted Gin Lane in 1751 (claimed by some to show a young girl with FAS), Sir Francis Bacon, himself a judge and perhaps echoing the biblical Judges, was said to have been warning women against any alcohol consumption at all during pregnancy.

The first published instance in the modern era of the link between excess alcohol and infant health was made in 1899 by a physician who compared pregnancy outcomes in 120 of his alcoholic patients with 28 blood relatives. He found the former had a 20 percent higher infant death rate. In 1973, two Seattle physicians, Jones and Smith, authored a peer-reviewed article that first named and described fetal alcohol syndrome. A year later, they recommended that their pregnant alcoholic patients consider abortion as an alternative to the perceived risk of having a child with FAS, a position they maintained in spite of criticism that their claims lacked evidence.

As a starting point, it seems reasonable to assume that the fetus must be protected from alcohol’s effects by the body of its mother to some degree. After all, the mother’s liver processes her blood before passing it on to the fetus. There is no direct mixing of the blood of the fetus and the mother, and the baby does not have priority for the blood’s contents. But a mother’s liver cannot instantly metabolize all the alcohol it receives. It takes time, and during that time alcohol in the blood will be absorbed by the fetus. It is also reasonable to assume that at whatever level, alcohol’s effects on a fetus will be stronger than its affects on its mother. Once it grows beyond the immediate point of conception, and especially when it begins showing a pulse, we assume the fetus’ extreme chemical vulnerability until birth. That is primarily because, if we disregard the difference in races (such as the Chinese and Native Americans, both of whom tend to lack a genetic mutation that allows for efficient metabolism of alcohol) we know that in general, the larger the body, the more alcohol it can take, partially because its stomach can hold more food, which acts to slow alcohol absorption. The fetus is much smaller than its mother, so the comparison is a likely a valid enough one. (Taking races into consideration, from 1981 to 1991, reported rates of FAS generally mirrored the rates of alcoholism: Native Americans had the highest reported rates, followed by African Americans, Hispanics, Caucasians, and Asians. There is no reason to suppose those rates have changed markedly for the better in the ensuing years.)

Testing

The problem in FAS testing has always been how to determine exactly what a fetus’ vulnerabilities are, specifically whether they are linear, i.e., dose-dependent: the measurably more alcohol, the measurably worse the effects. (By contrast, the effects of the drug L-dopa on the human brain are non-linear, being independent of the dose.) Laboratory experiments were devised and continue to be improved, but of course there is a fundamental problem: experiments to measure such effects cannot ethically be done in classic laboratory conditions with mothers and their fetuses as test subjects. Also, in collecting statistical data from population studies, respondents can be unreliable in their self-reporting of alcohol consumption, and very likely will conceal other risk behavior as well, such as illegal or prescription drug use, smoking, and poor nutrition. However, clinical testing with animals has been done successfully and continues to show promise (Bakhireva). At least one such study involving sheep showed that for a given animal of known body type and health, alcohol as a teratogen will be dependent on the quantity, frequency, and timing of the fetus’ alcohol exposure. Thus, alcohol’s effects on fetal development appear at least not to be predictably non-linear, and although that is not quite the same thing as saying that the effects are linear, they are linear enough to have warranted increasingly detailed experiments. Different animal models, ranging from worms to fish to birds to (as above) sheep offer a range of advantages that are not reduced by the lack of direct human-body testing and direct human-fetus monitoring. The right animal for the right kind of test to answer specific questions about alcohol and fetal development has been shown to be an invaluable part of the science of fetal-alcohol testing. Each animal has its own particular benefit.

The key benefit in this kind of experimental model lies in allowing us to compare animal controls with animal test-subjects, note the latter’s abnormality in brain and body development, determine or conjecture the resultant symptoms, and then look for those symptoms in children or adults suspected of FAS. As an example, problems in the development of kidneys, ears (inner and exterior), eye-blink conditioning, and spatial learning problems, confirmed in tested animal-models, have also been identified in humans. One effect of alcohol for which no protocol has been successful is the uniform development of FAS over multiple animal species. Mice have shown FAS facial characteristics, but they do not survive parturition. Others show neural deficits but no facial characteristics or growth retardation. It seems that no one animal model will do.

Thanks to clinical testing, alcohol is now accepted as a teratogen. One study concluded that in the U.S. there may be as many as 10,000 – 20,000 new FAS cases a year. FAS’s facial characteristics are pronounced but not defining in and of themselves, as normal children may have one or several of them: low nasal bridge, epicanthal fold, “railroad track” ears, indistinct philtrum, short palabebral fissures, flat mid-face and short nose, thin upper lip, micrognathia. Behavior abnormalities are a magpie’s nest of symptoms, most of them perfectly descriptive of non-FAS children, adolescents, and adults: hyperactivity, stubbornness, impulsiveness, passiveness, fearlessness, irritability, sleep difficulties, teasing or bullying of others, hypersensitivity to sound and touch, difficulty with change, organizational difficulties, poor self-image, overstimulation difficulties, depression or withdrawal, problems with truancy, problems with sexuality (“Texas Adoption Resource Exchange”). There is also the term fetal alcohol effects (FAE), harder to diagnose with symptoms matching a wide array of possible causes. (Fetal alcohol spectrum disorders is another evolving umbrella term, but is not a diagnosis.)

FAS: Moral Panic?

There has been an extensive educational campaign against FAS, and in the U.S., every bottle of beer, wine, or hard liquor that is sold must have a warning label: According to the Surgeon General, women should not drink alcoholic beverages during pregnancy because of the risk of birth defects. American pregnant women are warned that there is no minimum safe dose of alcohol, and told unequivocally that FAS is the leading cause of mental retardation. Yet these views are not universal. For example, in 2006 the British Royal College of Obstetricians and Gynaecologists stated that it is safe to drink one or two standard units (which vary with the type of alcohol) up to twice a week. A Danish study is considerably more liberal, indicating that moderate drinking early in pregnancy — about a drink a day — had not harmed intelligence, attention or self-control in five-years-olds. So there is clearly no universal standard. Why?
In 1999, two scholars published Fetal Alcohol Syndrome: The Origins of a Moral Panic, claiming that FAS had all the hallmarks of hysteria similar to the day-care sex-abuse trials in the 1980s and 1990s. Thirteen years later that article is still one of Oxford Press’ Journal of Alcohol and Alcoholism’s most-read articles (Armstrong, and Abel). In it, the authors write that in colonial times alcohol consumption was four times higher than today, yet there was no sign of FAS. They write of an inherent conflict of interest for clinicians who have much to gain in funding by fudging their figures to indicate a problem larger than it is. This is done by estimating thresholds of toxicity downward, thus making the problem potentially more widespread. Rates of drinking following different patterns are averaged together instead of separating them. For example, a pregnant woman who has one drink per day is lumped together with a pregnant woman who has seven drinks one day a week, with the latter pattern being the only one likely to induce actual FAS. They point out that the demographics of FAS are ignored: FAS for Native- and African-Americans, who have markedly higher rates of alcoholism (noted above), are extended to whites and Asians because “Liberal-minded social scientists are especially wary of associating a stigmatized behaviour with race or class, because such associations perpetuate discrimination.” Their goal was to democratize FAS, and for those who know no better, they did.

Women who normally drink in moderation should feel no need to become temporary teetotalers while pregnant, because alcohol in moderation is good for them. But alcoholics and binge-drinkers should not become pregnant in the first place until they solve their problems.

Works Cited

“A closer look at Fetal Alcohol Syndrome.” Texas Adoption Resource Exchange. Texas Department of Family and Protective Services, n.d. Web. 22 Oct 2012. <http://www.dfps.state.tx.us/Adoption_and_Foster_Care/About_Our_Children/Disabilities/fetal_alcohol.asp

Armstrong, Elizabeth, and Ernest Abel. “Most-read articles during September 2012.” Alcohol and Alcoholism. n. page. Web. 22 Oct. 2012. <http://alcalc.oxfordjournals.org/reports/most-read>.

Bakhireva, Ludmila. “Focus on: Biomarkers of fetal alcohol exposure and fetal alcohol effects.” Alcohol Research & Health. 34.1 (2011): n. page. Print. <http://pubs.niaaa.nih.gov/publications/arh341/56-63.pdf>.

Sanders, J. L. “Were our forebears aware of prenatal alcohol exposure and its effects? A review of the history of fetal alcohol spectrum disorder.” Canadian Journal of Clinical Pharmacology. 16.2 (2009): n. page. Web. 22 Oct. 2012. <http://www.ncbi.nlm.nih.gov/pubmed/19439773>.