Research suggests young drinkers

Let’s face it. This St. Patrick’s Day you’re probably going to drink. On Saturday, when cases of your favorite pale ale line your friend’s Allston apartment, you may consume one or two or 10.

But a recent study linking young drinkers with lower brain cell counts may make you think twice about downing bulks of brew.

Everyone knows drinking is “bad,” and long-term binge-drinking can cause liver damage and even mild impairment of motor skills. But cirrhosis of the liver won’t kick in for years, and young brains are more resilient than older brains.

Right?

Wrong. New research suggests young drinkers are flirting with disaster. According to a group of doctors at the University of North Carolina, youth drinking can result in semi-permanent as well as permanent brain damage — more than any other age group.

Dr. Michael De Bellis at the University of Pittsburgh Medical Center performed Magnetic Resonance Imaging tests on subjects ages 14-21 who abused alcohol to compare their hippocampi, a central structure of the brain that governs some learning and memory, to those who have abstained from alcohol. He found that the difference between the brain size of normal teens and alcohol abusers neared 10 percent.

And the younger the brain, the more risk for damage exists, according to Dr. Fulton Crews, professor of pharmacology and psychiatry at UNC.

“We don’t exactly understand why the brain damage occurs,” Crews said. “But through brain imaging and animal studies we have linked smaller brains with binge drinking.”

Dr. Scott Swartzwelder, a Duke University neuropsychiatrist demonstrated alcohol consumption poses significantly higher risks to younger drinkers. His findings show adolescent drinkers will suffer significant learning impairment and memory loss from very small amounts of alcohol, yet will become less sedated than adults.

Swartzwelder’s study compared how alcohol consumption in young adult rats and adult rats affects the hippocampus. Learning depends on interaction between nerve cells and the hippocampus.

Swartzwelder gave both the adult and young adult rats large quantities of alcohol and tested how that affected their memorization of maze patterns. He found the younger rats’ performance markedly more impaired than the adult rats.

“We don’t exactly know why young brains are more susceptible to alcohol-induced hippocampus damage, but we’re studying it,” Swartzwelder said.

Swartzwelder then tested his theory on humans and found that a group of volunteers ages 21-24 years old were able to learn 25 percent less then a group age 25-29.

“The damage was severe,” Swartzwelder said. “My group of scientists also tested the long-term damage done by youth binge drinking and found that to be measurable as well. It’s no joke — the younger you are when you drink, the more brain damage you’re going to incur.”

What literally happens in the brain while learning is that nerve cells, or neurons, launch electrical signals from the cell’s center through its axons, an elongated part of the nerve cell. The axon then releases chemical messengers called neurotransmitters that bind to receptors on the receiving limbs of adjacent cells. The receiving cell is then either jarred into action or eased into rest depending on the type of neurotransmitter released by the axon. And for the actual memory to kick in, the cells of the hippocampus must actually undergo a physical change, which researchers assume occurs in synapses, the spaces between neurons that neurotransmitters cross over. Basically, the more neurons move through the same place, the heavier the mark they leave is. This is called long-term potentiation, a process Swartzwelder found alcohol consumption hinders.

Long-term potentiation — memory production — involves a neurotransmitter called glutamate, which strengthens a cell’s electrical stimulation when it binds to the receiving end of a cell, a NMDA receptor. The study discovered that chronic alcohol leads to supersensitive glutamate NMDA receptor responses, particularly glutamate-NMDA mediated delayed neuronal death and nitric oxide formation, or brain damage, commonly referred to as “wet brain” by alcoholics.

According to Crews, evidence that youth binge-drinking, consuming about five drinks or more in one sitting, causes brain damage, is mounting.

“We know that adults who drank as teenagers have smaller brains, but we don’t know why,” he said.

According to Crews, some of the brains cells lost from binge-drinking can regenerate, but they may not be as “strong” as previous cells before damage.

Crews said not only are adolescent hippocampi more vulnerable to alcohol-induced damage, but that because younger people seem to pass out at higher blood-alcohol levels, they will therefore consume more alcohol in general.

“We don’t exactly understand the mechanism, but it takes more alcohol for a younger person to pass out, Crews said. “And obviously if you’re passed out you’re not going to be able to consume alcohol.”

Boston University Medical Center, in a joint effort with the National Institute of Alcohol Abuse and Alcoholism, is one of over 20 nationwide schools to begin recruiting volunteers for a new study that will explore different treatment for alcoholism.

The study will test how well different combinations of medication and psychotherapy help alcoholics, including one FDA-approved drug and one drug used in Europe.

The NIAAA website indicates that nearly 7 million youths between the ages of 12 and 20 binge-drink at least once a month. According to the Harvard School of Public Health, two out of every five college students binge-drink regularly.

According to Swartzwelder, the amount of damage done by adolescent binge-drinking is unforeseen.

“If 10 percent of millions of people’s brain power is lost from alcohol, we may never know how much we have hindered our progress as a society,” Swarzwelder said.