Alcohol, Adolescence, and the Brain

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        Blurred vision, impaired motor coordination and memory, and slurred speech are characteristics that clearly demonstrate that alcohol affects the brain. Adolescence is a time when people begin to use alcohol much more frequently. A survey of 70,000 people by the Center for Science in Public Interest has shown that 41.7% of people ages 12-17 have used alcohol in their lifetimes, and that the prevalence of binge drinking (five or more drinks in the same occasion) gradually increases from 3% at age 13, to 38% at age 20 (CSPI, 2000). Extreme intensities of alcohol consumption among adolescents is especially perturbing because a great deal of structural and function brain development occurs during this period. (Spears, 2002). Furthermore, evidence is increasingly suggesting that alcohol affects brain function and behavior of adolescents differently from adults, and that adolescents are extremely vulnerable to the long-term deleterious effects alcohol has on brain function and behavior.     

 Adolescence: A time of neural development      

As a person transitions from childhood into adolescence, dramatic changes in behavior occur and as this course has taught us, this change in behavior corresponds with changes in the brain. During adolescence, the brain is highly plastic and a substantial amount of synapses are eliminated or pruned in the cortex (Seeman, 1999). This translates to changes in the brain regions important for memory, voluntary motor behavior, impulse control, decision making, planning, and other cognitive functions: the frontal lobes. Frontal lobe gray matter volumes increase throughout childhood until age 12 and then decline during adolescence until they reach adult levels by age 16-18. Frontal lobe metabolism follows a similar pattern (Chugani, 1998). Furthermore, it is apparent a process called frontalization, or an increased reliance on the frontal lobes in the control of behavior, occurs during adolescence (Rubia et al., 2000). In addition, changes in other areas of the brain also occur. Gray matter volume in the occipital lobes, which plays a major role in processing visual information, increases throughout adolescence. Similarly gray matter volume in the temporal lobes, which are involved in memory formation as well as visual and auditory processing, are not fully developed until age 16-17 (Geidd et al., 1999). It has become evident that the adolescent brain is in a period of intense development of brain structure, brain function, and cognitive processes associated with these regions as mentioned above. Furthermore, scientific evidence has shown that alcohol differentially effects adolescent brain function during this sensitive period.                

 Differential effects of alcohol on adolescents and adults

      From stories we have heard from others, perhaps from our own experiences, or from keeping up with scientific research findings, it is well known that alcohol impairs learning and the formation of new memories. It is likely that alcohol produces these impairments by disrupting neural plasticity in brain regions involved in forming memories, such as the hippocampus. One model of encoding memories consists of changes in the brain brought by our experiences. This idea has been named long-term potentiation. Long-term potentiation (LTP) involves the long-lasting strengthening of a chemical synapse. In other words, when a patterned input (or something we are trying to form into a memory) repeatedly stimulates one cell, the cells that receive signals from this cell are more responsive when given the same patterned input to the original cell. This process has been associated with learning.                           

     Alcohol interferes with LTP processes. Increased amounts of alcohol will prevent the occurrence of LTP (corresponding to impeding learning), and studies have found the adolescent brain is dramatically more sensitive to the effects of alcohol on LTP than adults. For LTP to occur in the hippocampus, activation of a particular receptor called the NMDA receptor must occur. This allows calcium to enter the cell which sets off a chain of events that leads to long-lasting effects of the increased response of that cell, and LTP occurs. Alcohol has been shown to interfere with the activation of the NMDA receptor, preventing influx of calcium, which prevents the consequent changes that are part of LTP process, from occurring. Furthermore, research has shown that alcohol was significantly more effective in inhibiting LTP in immature verses mature rats.  Ethanol nearly blocked the induction of LTP in slices from immature rats (Swartzwelder et al., 1995). Corroborating evidence has been found in learning the water maze tasks in rodents. Compared to adult rats, adolescent rats showed significantly greater alcohol induced learning impairments of the water maze task (Markwiese et al., 1998).      

       Considering the similarities in the neurobiological mechanisms underlying memory formation between rats and humans, we can expect similar outcomes of increased human adolescent vulnerability to alcohol-induced learning impairments. However, due to ethical reasons of not being able to get humans drunk, sacrifice them, and then slice their brains for analysis, studies of this nature have not been conducted. Behavioral studies on human adolescents have shown that when given the task of being shown an image, asked to draw it right away, and then again 20 minutes later, alcohol inhibited performance in this task. When tested under placebos, all subjects including placebo and control groups performed equally. However when the placebo was switched to alcohol, subjects in this group performed worse in general, and subjects in their early twenties performed much worse than subjects in their late twenties (Acheson et al., 1999).                                                                         

       In sum, ethanol inhibits LTP to a greater degree in adolescent mice compared to adult mice to the point of nearly blocking LTP in adolescent mice all together. In humans, alcohol impedes performance on short term memory tasks in general, and to a greater degree in adolescents than in young adults. Long-term effects of alcohol abuse during adolescence            

       In addition to the cognitive learning and memory deficits described in the last section, research has given evidence for the potential existence of differential long-term effects of alcohol abuse on cognitive abilities during adolescence and during adulthood. Researchers have studied adolescents in an in-patient abuse treatment program who have been sober for at least three weeks after a period of frequent drinking. When compared to controls from the community, these adolescents performed worse on learning, memory, and visuospatial functioning tests (Brown et al., 2000). Other researchers have taken a longitudinal approach in examining this field of interest. Subjects were recruited from similar treatment programs, and then followed over the next four years after they left from such programs. A return to drinking was found to further deteriorate cognitive abilities (Tapert et al., 1999).  Furthermore, this same researcher followed subjects from the same treatment program over a period of eight years from ages 16-24. After performing cognitive tests throughout the eight years, it was found that the greater the cumulative levels of alcohol use, the greater the impairment of verbal learning and memory during the final test when subjects were in their mid-twenties (Tapert et al., 2002).  Additionally, taking this research to the next level, this scientist conducted fMRI neuroimaging scans on alcohol-dependent young women and healthy controls of similar age women during working memory tasks. It was found that alcohol-dependent young women exhibited significantly less neural activation while performing the task compared to controls (Tapert et al., 2001).  Also, MRI studies of hippocampal size in relation to adolescent alcohol abuse have been conducted. It was found that hippocampal size decreased in those who used alcohol as adolescents compared to healthy controls, and that the greater the alcohol use, the greater the decrease in size of the hippocampus (De Bellis et al., 2000).                                   

        From this research it seems that heavy use of alcohol during adolescence can have detrimental long term effects on brain function such as the amount of brain activation dedicated to a task, a permanent decrease in hippocampal size and deleterious effects of performance on learning and memory tasks. Continued drinking during adolescence corresponds to a continued decrease in cognitive abilities, and the greater the alcohol abuse is during adolescence, the greater these cognitive abilities are impaired.         

Summary     

       From this research it can be deduced that adolescence is a time of neural development. Our behavior as well as our brain is in the process of maturation. During this sensitive period, it seems that in adolescent mice, LTP, which has been associated with mechanisms for learning is severely inhibited, especially in comparison to adult mice. Given the similarity of the neurobiological mechanisms underlying learning and memory in rats and humans, these results most probably extend to humans. Behaviorally, adolescent humans exhibit increased learning and memory impairment in learning and memory tasks when exposed to alcohol. Furthermore, substantial alcohol abuse during adolescence appears to have long-term effects of decreased hippocampal size, levels of brain activation, and performance on learning and memory tasks.                      

Conclusion        

  Adolescents seem to be in a state of neural maturation and their nervous system seems to be especially sensitive to, and influenced by alcohol. Surveys have shown that there are high percentages of adolescents who binge drink. These adolescents are susceptible to the long-term impairment of vital cognitive abilities of learning and memory as well as long-term negative changes occurring in brain structures and functions. Apart from statistics on paper, we as college students see and experience this first hand for ourselves. I think this is reality for us and other people at this age because we are unaware of the long-term consequences alcohol can have on our body. The purpose of this paper is to spread this knowledge to other adolescents so that we are aware of such possible consequences as we live through this period of our lives. However, it is not being suggested to completely give up drinking. These studies were of those who binge drink and abuse alcohol. As we experience these times of our lives we should remember that alcohol is healthy and less harmful in moderation and that constant use and abuse may result in serious long-term consequences.       

References 

Acheson, S., Stein, R. & Swartzwelder, H.S. (1998). Impairment of semantic and figural memory by acute alcohol: Age-dependent effects. Alcoholism: Clinical & Experimental Research, 22, 1437-1442.

Brown, A.S., Tapert, S.F., Granholm, E. & Delis, D.C. (2000). Neurocognitive functioning of adolescents: effects of protracted alcohol use. Alcoholism: Clinical & Experimental Research, 24, 164-171.

Center for science and public interest. Adolescent alcohol use statistics: Key findings from the 2000 National Survey. http://www.cspinet.org/booze/FactSheets/2000_Adolescent_Alcohol_Use_Stats.pdf

Chugani, H. (1998). Biological Basis of Emotions: Brain Systems and Brain Development. Pediatrics, 102, 1225-1229.

De Bellis, M.D., Clark, D.B., Beers, S.R., Soloff, P.H., Boring, A.M., Hall, J., Kersh, A. & Keshavan, M.S. (2000). Hippocampal volume in adolescent-onset alcohol use disorders. Am J Psychiatry, 157, 37-744.

Giedd, J., Blumenthal, J., Jeffries, N., Castllanos, F., Liu, H., Zijdenbos, A., Paus, T., Evans, A. & Rapoport, J. (1999). Brain development during childhood and adolescence: a longitudinal MRI study. Nature Neurosci, 2, 861-863.

Markwiese , B.J., Acheson, S.K., Levin, E.D., Wilson, W.A. & Swartzwelder, H.S. (1998). Differential effects of ethanol on memory in adolescent and adult rats. Alcoholism: Clinical & Experimental Research, 22, 416-421.

Rubia, K., Overmeyer, S., Taylor, E., Brammer, M., Williams, S.C., Simmons, A., Andrew, C. & Bullmore, E.T. (2000). Functional frontalisation with age: mapping neurodevelopmental trajectories with fMRI. Neurosci Biobehav Rev, 24, 13-19.

Seeman, P. (1999). Images in neuroscience. Brain development, X: pruning during development. Am J Psychiatry, 156, 168. 

Spear, L.P. (2002). The adolescent brain and the college drinker: biological basis of propensity to use and misuse alcohol. J Stud Alcohol Suppl, 14, 71-81.

Swartzwelder, H.S., Wilson, W.A. & Tayyeb, M.I. (1995). Differential sensitivity of NMDA receptor-mediated synaptic potentials to alcohol in immature vs. mature hippocampus. Alcoholism: Clinical & Experimental Research, 19, 320-323.

 Swartzwelder, H. S., Wilson, W.A. & Tayyeb MI (1995). Age-dependent inhibition of long-term potentiation by alcohol in immature vs. mature hippocampus. Alcoholism: Clinical & Experimental Research, 19, 1480-1485.

Tapert, S.F. & Brown, S.A. (1999). Neuropsychological correlates of adolescent substance abuse: four-year outcomes. Journal of the International Neuropsychological Society,  5, 481-93.

Tapert, S.F., Brown, G.G., Kindermann, S.S., Cheung, E.H., Frank, L.R. & Brown, S.A. (2001). fMRI measurement of brain dysfunction in alcohol-dependent young women. Alcoholism: Clinical & Experimental Research, 25, 236-45. 

Tapert, S.F., Granholm, E., Leedy, N.G. & Brown, S.A. (2002). Substance use and withdrawal: neuropsychological functioning over 8 years in youth. Journal of the International Neuropsychological Society,  8, 873-83.

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