Eyewitness News on Demand May 21, 2012
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BYU Professor's Statement To Commission

Letter To Dept. of ABC from Professor Scott C. Steffensen, PhD, Professor and Principle Investigator, Brigham Young University

    Dear Commissioners,

    I write to inform you of some sobering facts regarding underage drinking in America. Alcohol use and abuse is widespread in our society. The economic and societal implications arising as direct or indirect result of alcohol consumption are staggering, with estimates ranging as high as $185 billion in the U.S., annually (Gordis, 2000).

    These economic costs are unsettling; however, they pale by comparison to the personal loss of life, not to mention the diminished quality of life for millions of Americans.

    The most recent statistics from the U.S. Substance Abuse and Mental Health Services Administration's National Household Survey on Drug Abuse indicate that nearly 7 million youths between the ages of 12 and 20 binge-drink at lease once a month. Just in regard to drinking and driving: One-half of all fatal car crashes among 18- to 24-year-olds involve alcohol and one-third of all seriously injured 18- to 24--year-olds are intoxicated.

    A 1997 longitudinal study revealed that the prevalence of alcoholism is directly correlated with the age of onset of alcohol drinking (Grant and Dawson, 1997). Restated more simply, the younger someone is when he begins to regularly drink alcohol, the more likely that individual will eventually become an alcoholic.

    Overall, beginning at age 14, the risk of future alcohol dependence decreased by 14 percent with each passing year of abstention from alcohol drinking. Moreover, after adjusting for history of alcoholism and other characteristics associated with early onset drinking, individuals who begin drinking before age 14 are about three times more likely than those who begin drinking after age 21 to be injured while drinking (Hingson et al., 2000).

    Scientists and the public alike have known for many years that there are severe consequences associated with underage drinking. According to Dr. Enoch Gordis, director of the National Institute of Alcohol Abuse and Alcoholism, the list includes, "interference with learning, social, and other competencies, fatal traffic crashes, injuries, homicide, suicide, and early, more frequent, and less safe sexual activity."

    We can now add to this list the converging lines of evidence providing a very compelling argument that alcohol is actually damaging the brains of adolescents that drink heavily and that they are more susceptible to alcohol-induced brain damage than mature adults. Because their brains are still developing well into their twenties, teens and young adults who drink excessively may be destroying significant amounts of mental capacity in ways that are more dramatic than in older drinkers.

    Teens and young adults who drink heavily sometimes joke that they are killing a few brain cells. The truth is even more sobering. Brain imaging and cognitive performance studies have revealed that heavy, regular drinking can damage the developing brains of teens and young adults and perhaps destroy brain cells involved in learning and memory (Taper et al., 2001).

    As stated by the authors of this study, "We think that it may be more dangerous for a 15-year-old to drink heavily than for a 20-year-old because the finishing touches on brain development haven't completed and could be interrupted or disturbed."

    Recent evidence indicates that underage alcohol drinking produces anatomical differences between the brains of healthy teens and alcohol abusers. Underage drinkers appear to be most susceptible to damage in the hippocampus, a structure buried deep in the brain that is responsible for many types of learning and memory, as well as the prefrontal cortex, located behind the forehead, which is the brain's chief decision maker and voice of reason.

    Both areas undergo dramatic change in the second decade of life. Michael De Bellis at the University of Pittsburgh Medical Center used magnetic resonance imaging to compare the hippocampi of subjects 14 to 21 years old who abused alcohol to the hippocampi of those who did not.

    He found that the longer and the more a young person had been drinking, the smaller his hippocampus (De Bellis et al., 2000).

    The average size difference between healthy teens and alcohol abusers was roughly 10 percent. Considering that teens have roughly 100 billion brain calls, these teens may he losing up to 10 billion of them, considerably more than a "few brain cells".

    If, as these studies suggest, heavy alcohol use during adolescence causes lingering cognitive deficits, and brain damage, adolescents who abuse alcohol may suffer consequences long after the abuse ends. Compounding the problem of alcohol-induced brain damage and cognitive defects is the fact that alcohol produces a "a lower sedative response" in the brains of adolescents (Crews et al., 2000). As a result, says the author, teenagers "can drink more and damage their brains more".

    The impetus to study the effects of underage drinking in people rose out of rat studies published by Scott Swartzwelder and his colleagues at Duke University (Swartzwelder et al., 1995). Six years ago, when Swartzwelder published his first paper suggesting that alcohol disrupts the hippocampus more severely in adolescent rats than in adult rats, "people didn't believe it," he says.

    Since then, his research has shown that the adolescent brain is more easily damaged in the structures that regulate the acquisition and storage of memories. He found that alcohol blocked long-term potentiation, a neuronal correlate of memory, in adolescent brain tissue much more than in adult tissue.

    Next, Swartzwelder identified a likely explanation. Long-term potentiation and thus memory formation-relies in large part on the action of a neurotransmitter known as glutamate, the brain's chemical king- pin of neural excitation.

    Glutamate strengthens a cell's electrical stimulation when it binds to a docking port called the NMDA receptor. If the receptor is blocked, so is long-term potentiation, and thus memory formation.

    He found that exposure to the equivalent of just two beers inhibits the NMDA receptors in the hippocampal cells of adolescent rats, while more than twice as much is required to produce the same effect in adult rats.

    These findings led him to suspect that alcohol consumption might have a dramatic impact on the ability of adolescents to learn. So he set up a series of behavioral experiments. His colleagues soon found that while sober younger and older rats performed equally well in memory tasks roughly akin to that performed by a human when remembering the location of his parked car, older rats, that had binged on alcohol as younger rats, performed much worse than older rats that had not been exposed to alcohol.

    To summarize, emerging evidence regarding the effects of alcohol on specific neuronal structures in the rat brain as well as epidemiological and imaging studies in human brains are providing a brush stroke of a picture of alcohol-induced long-term impairments produced by underage drinking.

    If further studies back up these findings, there may be a substantial case for campaigns to curb young people from drinking. If, as the evidence suggests, this age group is found to be especially vulnerable to alcohol and its long-term effects we may need to concentrate our efforts on preventative strategies.

    Sincerely,
    Scott C. Steffensen, PhD
    Professor and Principal Investigator (NIAAA grant "Neuropharamacological substrates of alcohol addiction")
    Brigham Young University


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