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Release: Sept. 22, 1999

UI study suggests variable effects of fetal alcohol syndrome on brain

IOWA CITY, Iowa -- Fetal alcohol syndrome in affected people has been associated with mental retardation and a smaller or nonexistent corpus callosum. The callosum is a major brain pathway that coordinates input from one side of the brain to the other to help provide unified sense perception. However, a study led by a University of Iowa Health Care researcher suggests that moderate (versus severe) alcohol overexposure can cause the corpus callosum to be larger than normal.

"Previous research showed that the corpus callosum is very small or even nonexistent in people with fetal alcohol syndrome," said Michael W. Miller, Ph.D., UI professor of psychiatry and pharmacology, and a career research scientist at the Iowa City Veterans Affairs Medical Center. "But this human data was quite at odds with other studies, including one at the UI involving rats, which showed maternal alcohol intake can increase the number of cells contributing connections passing through corpus callosum in offspring."

The contradiction motivated Miller and two University of Washington researchers to investigate how fetal alcohol syndrome affects the corpus callosum in macaques, primates that closely resemble humans. The team analyzed 15 post-puberty macaques affected to varying degrees by maternal alcohol consumption during gestation. The findings were published in the Sept. 13 issue of the Journal of Comparative Neurology.

Using magnetic resonance imaging (MRI) and post-mortem analyses, the team found that offspring of macaque mothers fed 170 - 270 milligrams (mg) of alcohol per deciliter of blood (sufficient to bring blood alcohol concentrations to .17 to .27 mg percent) for several weeks or months had more axons in their corpus callosums than did control animals. These axons conduct signals from one side of the brain to the other. In contrast, Miller said, the research on humans affected by fetal alcohol syndrome was generally based on extreme cases in which the mothers' blood alcohol levels were closer to 300 mg per deciliter of blood or .30 mg percent blood alcohol level.

"The human data compiled to date has been highly selective and almost biased to worst-case scenarios," Miller said, referring to the .30 blood alcohol concentration. "Our findings suggest that moderate alcohol overexposure causes an increase in the number of axons, whereas high alcohol overexposure causes a breakdown, thus reducing the size of the corpus callosum."

Miller said human clinical studies under way at other institutions may confirm this difference between callosal hypergrowth and hypogrowth.

"One particularly interesting finding in our study was that the alcohol overexposure did not increase the entire corpus callosum but mostly enlarged the rostral portion, the part toward the front of the head," Miller added. "This portion of the corpus callosum communicates information between the frontal and parietal cortexes, the brain areas that participate in movement and touch and in executive functions such as initiating voluntary movements and other higher-order processing."

Several behavioral studies on children with fetal alcohol syndrome show that executive functions of the rostral portion are reduced due to the alcohol exposure.

Miller said that although the primate and human clinical studies differ on the effect alcohol has on corpus callosum size, the studies agree that the part most affected is the rostral portion.

He described his findings as "more provocative than coming up with any solutions." He hopes his study will encourage researchers conducting human studies to study a range of people affected by fetal alcohol syndrome.

"There might also be a way of using the MRI analysis in clinical settings to better see how children are affected," he added. "The findings could possibly help other researchers find ways for these children to learn more effectively."

Miller will next investigate callosal projection neurons to understand the factors that regulate the growth of these cells and how alcohol exposure affects them.

Miller's co-investigators from the University of Washington were Susan J. Astley, in epidemiology at the School of Public Health and Community Medicine, and Sterling K. Clarren, in pediatrics at the School of Medicine. Miller's work on the study was supported in part by a grant from the federal Department of Veteran Affairs. All three researchers received grant support from the National Institutes of Health (the National Institute of Alcohol Abuse and Alcoholism, and the National Institute of Dental Research). The University of Washington researchers also received support from General Electric.