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Alcoholism and alcohol abuse are universal problems with various precursors. The effects, physical, cognitive, social and biological, are unmatched. The medical research community continues its battle with society on the blatant health effects from alcohol consumption. More importantly, professionals are worried about the effects of alcohol use in adolescents. The results are clear, but for some reason they are not convincing the most stubborn portion of the population: teens.

            Of the many effects that alcohol consumption has on the brain, Jaime Roitman focuses on decision-making associated with risks. The prefrontal cortex is involved with this task and undergoes a lack of maturation and development when doused with alcohol. Roitman experimented with rats and looked at how the orbitofrontal segment in the prefrontal cortex was stressed when the subjects had to make decisions resulting in various sized rewards and having different possibilities. She fed the rats gelatin containing ethanol based on their experimental group: control, low or high. The ethanol-high group received enough gelatin to categorize them as binge-drinkers. Once the rats reached adulthood, their behavior was tested in regard to risk preference. Activity in the orbitofrontal segment was recorded using an electrophysiological recording to observe the corresponding neurons. Her results showed that the high-ethanol rats had a greater preference towards large, risky rewards than small, certain rewards. The control and low-ethanol rats did not. This data clearly showed that excessive alcohol consumption is correlated with risk behavior and preference.

            In a birth defects research study, Tapia-Rojas et al. reviewed the various consequences of alcohol consumption in adolescence, focusing on mitochondrial damage. They noted that binge-drinking patterns are associated with depression because of a mechanism implicating that hippocampal neural progenitor cells are dying which results in a decrease of adult neurogenesis. Their own research, included in the review, indicates that the mitochondria play an important role in alcohol toxicity during binge-drinking episodes. The damage to mitochondria can progress overtime and can have lasting effects well into adulthood, even if the subject has stopped drinking. In 2017, Tapia-Rojas et al. evaluated the hippocampus of rats with a single binge-drinking episode and found that it induced a rapid oxidative response 1 week after treatment. Reduced ATP was also reported and indicates a loss of the bioenergetics function of the mitochondria over time.

            Heikkinen et al. conducted a longitudinal study on excessive alcohol use and its relation to the volume of grey matter. Thirty-five heavy drinking teens and twenty-seven light-drinking control teens filled out a follow-up survey 3 times throughout 10 years after their initiation in the study. At the 3 testing points, grey matter volume was recorded and compared between the two experimental groups. They found that grey matter volumes were smaller in the heavy-drinking subjects in the bilateral anterior cingulate cortex, right orbitofrontal and frontopolar cortex, right superior temporal gyrus and right insular cortex. The control group did not see such significant decreases in volume in these areas. This data makes it clear that excessive alcohol consumption is correlated with an abnormal development of the brain’s grey matter. These structural changes might reflect a subject’s reduced sensitivity to the negative effects of alcohol use.

            These three studies all focus on how alcohol use in young adults affects their brain development and consequently their behavior in adulthood. Roitman’s work looks directly at the behavioral consequences. Tapia-Rojas et al. and Heikkinen et al. examine long-lasting effects on binge-drinking. All three studies highlight the negative effects of alcohol consumption on the adolescent population, reminding us that the most important part of our body, the brain, can be underdeveloped and changed permanently due to alcohol abuse. Heikkinen et al. focuses on the brain structure that changes overall, Tapia-Rojas et al. focuses on the cell mechanisms altered from consumption and Roitman’s study focuses on the behavioral consequences due to a change in brain chemistry in specific parts of the brain. It’s interesting that countless amounts of research have been done on this subject, but society seems to not have changed much from it. The data is there, but our minds are elsewhere.

Works Cited

Heikkinen, Noora, et al. “Alcohol Consumption during Adolescence Is Associated with Reduced Grey Matter Volumes.” Addiction, vol. 112, no. 4, 2017, pp. 604–613.

Mcmurray, Matthew Stephen, et al. “Consequences of Adolescent Ethanol Consumption on Risk Preference and Orbitofrontal Cortex Encoding of Reward.” Neuropsychopharmacology, vol. 41, no. 5, 2015, pp. 1366–1375.

Tapia-Rojas, Cheril, et al. “Alcohol Consumption during Adolescence: A Link between Mitochondrial Damage and Ethanol Brain Intoxication.” Birth Defects Research, vol. 109, no. 20, 2017, pp. 1623–1639.