New Clues to Alcoholics' Sleep Problems

Researchers discover cellular differences in monkeys

WEDNESDAY, Oct. 27, 2004 (HealthDayNews) -- Alcoholics complain that their sleep is disrupted when they quit drinking, and they often return to their addiction to coax some shut-eye.

A new study backs up that complaint, and offers new hope for a drug that can help keep them sober.

Researchers have pinpointed changes on a cellular level that may be responsible for that sleep disruption, a discovery that may help them intervene with a medication to normalize sleep in recovering alcoholics.

In the research, a team led by Dwayne Godwin, a senior researcher at Wake Forest University Baptist Medical Center, found that monkeys who chronically drank alcohol had a fourfold increase in one of the genes that express calcium channels -- proteins that generate brain rhythms associated with normal sleep.

"Part of the sleep disturbance can be explained by the increase in gene expression," Godwin said, explaining that this calcium channel is suppressed by alcohol.

The findings were presented Oct. 27 at the Society for Neuroscience's annual meeting in San Diego.

"By understanding the role of this calcium channel, doctors might be able to pick a drug that normalizes sleep, that compensates for the effects on the calcium channel," Godwin added.

There are many types of calcium channels, but the type studied is one that is most active when the brain is less active, such as during sleep.

Based on the new study, Godwin and his colleagues speculate that what is happening is a compensatory mechanism: that the gene overproduces copies of the calcium channel to make up for the deficit that accompanies heavy drinking.

But the overproduction of the genes didn't lead to an increase in working calcium channels, he found, and the cells still had disturbances in the channels. Compared to the teetotaling monkeys, the heavy-drinking monkeys were more active at night, probably reflecting disrupted sleep, he said.

The practical application of the research, Godwin said, is to help those who treat alcoholics understand the nature of the sleep disruption. "In the clinic, one of the greatest elements leading to return to drinking is disruption in sleep," he said. In the social or casual drinker, alcohol initially acts as a sedative, making sleep come easier. But in chronic alcohol users, the brain develops a tolerance to alcohol's sedative effects, and the restorative stages of sleep decline.

In response, chronic users may raise their intake to try to improve sleep. When alcohol is stopped, the brain doesn't return to normal right away, or may never return to normal, and sleep problems can worsen, Godwin said.

Other sleep experts say the study breaks new ground, and that it may be a promising start to solving recovering alcoholics' sleep problems. "This is the first model I am aware of showing how alcohol modifies gene expression," said Dr. Michel Cramer-Bornemann, staff physician and sleep specialist at the Minnesota Regional Sleep Disorders Center.

Further studies are needed, he said, to determine if the modification is clinically important or not.

"Understanding the mechanism of gene expression allows us to come up with treatments focused on where the problem lies," Cramer-Bornemann said.

Prescribing sleeping pills for alcoholics who have sleep problems often doesn't work well, Cramer-Bornemann said. "They don't respond because the effect of the alcohol that has been in the system for a long period of time makes them less sensitive to the medications," he explained. And some prescription sleeping pills are known to be addictive, not ideal especially for a patient trying to kick an alcohol habit, he added.

"This research has the potential to come up with alternative means of treating sleep problems in alcoholics," he added.

Dennis A. Twombly, program director for neurophysiology and pharmacology at the National Institute on Alcohol Abuse and Alcoholism, said the new research sheds light on which cellular changes occur in the brain with chronic alcohol consumption. "The big question that remains to be answered," he said, "is that, given we have these changes at the cellular level, more research needs to be done to establish the link to behavior."

More information

To learn more about healthy sleep, visit the National Sleep Foundation.

SOURCES: Dwayne Godwin, Ph.D., associate professor, neurobiology and anatomy, Wake Forest University Baptist Medical Center, Winston-Salem, N.C.; Dennis A. Twombly, Ph.D., program director, neurophysiology and pharmacology, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Md.; Michel Cramer-Bornemann, M.D., staff physician and sleep specialist, Minnesota Regional Sleep Disorders Center, Minneapolis; Oct. 27, 2004, presentation, Society for Neuroscience annual meeting, San Diego
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