Nov. 15, 1999 (Tuscaloosa, Ala.) -- A study funded by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) may have found a common pathway to explain the similarities between two childhood conditions -- attention deficit hyperactivity disorder (ADHD) and fetal alcohol syndrome (FAS).
Prenatal exposure to alcohol has long been known to cause mental retardation and has previously been linked to ADHD. The current study shows that rat pups exposed to alcohol while in their mother's wombs have less activity in their brains of a chemical transmitter called dopamine.
Our brains are composed of billions of nerve cells called neurons. We are able to think and act because those neurons communicate with each other by way of chemical messengers called neurotransmitters. Dopamine is one of those neurotransmitters.
The study, by Roh-Yu-Shen, PhD, senior scientist at the State University of New York at Buffalo, involved giving pregnant rats varied doses of alcohol during pregnancy. Shen and her research team found that the alcohol-exposed rat pups had 50% decreases of the activity of dopamine neurons in their brains. Furthermore, the decrease persisted as the pups matured into adult rats.
"This is a very interesting finding within a very important field of study," says Jaime L. Diaz-Granados, assistant professor at Baylor University. "The finding has serious implications for both children with FAS-induced ADHD as well as those children whose ADHD is not FAS induced. For the later group, we may find there are some dopamine abnormalities underlying ADHD."
The implication is that new drugs might be developed to help children with this disorder. "We have no treatment for children with fetal alcohol syndrome and we certainly need one," Kenneth Jones, MD, the researcher who first discovered FAS, tells WebMD. "If this decrease in the number of dopamine neurons in rat pups with fetal alcohol syndrome also occurs in human children, then a drug ... could be developed and might be helpful in treating these kids." Jones is a professor of pediatrics at the University of California, San Diego.
"Understanding how fetal alcohol exposure can contribute to ADHD allows us to understand the cellular mechanism of what's happening in the brain," Shen says. "We need to understand how to restore dopamine activity. We already know that stimulants like Ritalin can restore deficits in dopamine systems. Now we need to fine-tune that strategy in terms of different drugs and dosages."
Jerry Sells, MD, professor of pediatrics at Oregon Health Sciences University School of Medicine, has misgivings about that claim. "It is a big leap of faith to take anything we see in the rat model and apply it to what we see in children. We should be cautious using stimulant drugs on FAS kids."
"The ADHD symptoms that we see in FAS kids may not even be caused by the same basic mechanisms," Sells tells WebMD. "There are lots of neurotransmitters in the brain. I don't necessarily agree that the ADHD that we see in fetal alcohol syndrome kids is totally equivalent to the ADHD that we see in non-fetal alcohol kids. Both groups have some of the same symptoms, but they are not identical syndromes.
"Ritalin, for example, which helps many ADHD kids control their hyperactivity and concentrate, doesn't seem to be all that useful for FAS patients," continues Sells. "We may, indeed, be looking at some kind of common pathway but, because these were rat experiments, we're not sure that things happen in the same way in humans."