How detrimental is the impact of alcohol consumption on adolescent brain development and function?

The profound effect of alcohol on the intricate balance of chemicals and structures of the human brain has now been extensively explored for decades; gradually forming a core of scientific research enabling the accurate diagnosis of a spectrum of diseases, ranging from dementia to cancer. Despite this progress, there exists a gap in the way of definite and proven analysis on the impact of alcohol on a very susceptible group of people – the youth. An area of constantly developing theories and emerging concepts, the need to answer this question has never been greater – partly due to the more scientific mechanisms to be discussed later on in the paper, but also because heavy drinking is now a common practice amongst masses of adolescents around the world. According to the study conducted by Monitoring the Future in 2013, 69% of US students have reported alcohol use by the the time they graduate high school, and perhaps more conclusively, 24% of those in Grade 12 (17-18 year olds) endorse the activity of binge drinking. This paper will aim to justify that, on balance, the neurological impact of alcohol use in these adolescents can, in many situations, be very detrimental, and will extend this argument with pivotal areas for action in the future.

Examining the existing sources of biological literature, it becomes transparent that the general consensus amongst the global scientific community is that the consumption of alcohol during the developmental period of the human body can have long-term impacts – both in the context of structure and function. A critical facet of the brain that has been investigated is the size of the hippocampus – a small, curved formation located in each cerebral hemisphere (left and right sides of the brain) that plays a major role in  both the learning of new information, and the subsequent consolidation of memories. One of the earliest probes into the link between adolescent alcohol use and hippocampal volumes uncovered that when a group of adolescents and young adults with diagnosed alcohol use disorders (AUDs)  in the age group of 13-21 were set against demographically allocated controls, not only were smaller hippocampal volumes reported in those with an AUD, there was also a negative correlation between the size of the hippocampus, and the duration of alcohol abuse (De Bellis et al., 2000). In theory, taking into account the function of the hippocampus, this pointed towards a potential long-term impairment of memory function, a serious cause for concern.

The study itself was conducted by eight researchers, with the lead Michael de Bellis being a past medical student at the University of New York at Brooklyn, and having published multiple papers spanning throughout the last thirty years with a key focus on neurocognitive functions within young people (Duke Institute for Brain Sciences, 2019). This confirms his own very specific expertise within the field, and the highly reputable nature of the site of publication (NCBI, 2000), in conjunction with the fact that similar results were reproduced five years later (Nagel et al., 2005) further enhances the validity of the primary research undertaken in 2000.

Complementing this recognition of clear structural differences, current literature is also home to research in relation to the function and performance of the brain. Seven years prior, Nichols and Martin (1993) had investigated physiological brain function in adolescent heavy drinkers by measuring brain waves that form in response to an unexpected event i.e. a stimulus. The pair specifically examined the P300 brain wave, which typically occurs roughly 300 milliseconds after the stimulus in question. The adolescent subjects were asked to look at a series of depictions of common events, interspersed with images of what Nichols and Martin called ‘’oddball’’ events, in this case accident scenes in the midst of normal, driving stills. Under both the influence of a placebo and and a sedative (benzodiazepine), the P300 wave took longer to appear in the adolescents than in demographically comparable non-heavy drinkers, alluding to a clear neurological deficit in the process of handling and acting upon information. The use of both the placebo and sedative increases the legitimacy of the conclusions that can be drawn from the results, for it alludes to the effect of alcohol being the deciding factor. This alongside the knowledge of JM Nichols as an academic within the psychology department at University of Tasmania in Australia (NCBI, 1993) further adds to the credibility of the technique used.

On balance, although pre-existing sources can direct someone towards evidence of detrimental impact, further analysis of previous records is needed to truly evaluate how alcohol consumption can affect the brains of young people on a permanent basis – this paper will now attempt to isolate the vital pieces of available research in order to justify that adolescent alcohol consumption can create permanent and long-lasting defects beyond initial consumption.

Firstly, a prime illustration of this argument lies in the study conducted by Brown and his colleagues (2000) which examined 33 alcohol-dependent adolescents aged 15 and 16. When matched up with a control group on age, gender, education and socioeconomic status, the investigative team found that after 3 weeks of abstinence, the alcohol-dependent adolescents performed worse on both nonverbal and verbal memory tests, and demonstrated poorer visuospatial functioning. However, the critical discovery from this study that has not been replicated in many others is that the damage on the regions of the brain responsible for dealing with the tests used was so severe that despite the period of abstinence that the heavy drinkers partook, it could not allow them to perform on the same level as the non-drinkers. This uncovers a hint of the level of long-term damage that was inflicted as a result of the alcohol consumption, and develops the argument further. However, it must also be noted that the adolescents in question in this study had used alcohol an average of 753 times in their lives. Though the pressure of consuming alcohol at a younger age may be on the rise particularly in Western society, such numbers are not common today, and so this must be accounted for when analysing these results.

Moreover,  the impact on the brain is likely to be longer-lasting because during this time, the brain is still maturing. The prefrontal cortex of the brain is a region implicated in personality expression and decision making, but is in fact one of the last regions of the brain to develop, and is indefinitely within a critical period in all adolescents. The PFC is also however one of the most susceptible components of the brain in relation to damage from alcohol consumption (De Bellis et al., 2005), with significantly smaller grey and white matter volumes being reported within it (grey matter contains the brain’s neuronal cell bodies, whereas white matter contains relatively more long-range axon tracts). If the parameters of the question were to be expanded, an issue can clearly be seen in the potential of this PFC damage on the lives of young people in general, for during a time in which they make numerous social, economic and educational decisions that will largely shape the remainder of their lives, a negative influence on their ability to make rational decisions can easily create longer term ramifications.

Alternatively, it is also credible to convey the fact that there is a high level of variability in terms of the development of these disorders, and that not all adolescents who consume alcohol in large quantities will experience similar levels of impairment – some may show no evidence of brain damage at all. Reasons for this inconsistency include family history, for example. The development of AUDs is often influenced by genetics, and this too has been a focal point of existing research – the ERP study referenced earlier on in the paper was also assessed by Hill and Shen (2002), who concluded that children of alcoholics are more likely to be delayed in developing normal P300 patterns. Again, there is no true biological mechanism of yet to describe this relationship, but the pattern of family history playing a role in the development of alcohol disorder related diseases is progressing. Another factor is that of gender – women have been found to be more vulnerable to the toxins found in alcohol in terms of their effect on the brain (Hommer et al. 2001), but there currently remains insufficient evidence to draw conclusions upon in the realm of gender fluctuations amongst adolescents.

The closing argument this paper will present is based of our sensitivity to alcohol. The specialist term of ‘’sensitisation’’ refers to the concept that as alcohol consumption increases, the response and the reinforcing effect of drinking it increases in power, and the behavioural changes that usually follow e.g. aggression and further intake become amplified. One possibility that could be confirmed in the future with increased research is that as adolescent brains are still in a maturation phase and not fully developed, this sensitisation effect is more likely to be potent and occur – this will only lead to increased consumption, and higher chances of developing alcohol disorder related diseases.

To conclude, the arguments made throughout this paper have justified that excessive alcohol consumption in adolescents can create highly detrimental issues in the brain. Undeniable and proven changes to the structure of the complex network alongside the numerous examples of how its function can be altered highlight and distinguish this relationship as a strong one. The essential distinction however between this relationship and that of adults is that the intricate sub-structures of the brain e.g. the prefrontal cortex develop throughout childhood, and thus altering this process is more likely to lead to permanent effects than drinking at an older age. Expanding on this judgement, it is clear that more research is needed into the relationship between adolescent alcohol use and brain function  – research into the subject is in its initial phases, but with the number of adolescents drinking at potentially harmful levels, it is pivotal the process is sped up via enhanced funding and attention to attain the same level of knowledge known regarding adult AUDs. For example, though numerous studies were referenced in this paper alone, many were from very early on in the global scientific investigation – with the advancements in imaging techniques that have taken place more recently, studies need to be conducted as soon as possible in order to better understand the true biology of how exactly adolescent drinking can affect the brain. Though we are able to make inferences from experimental results, in order for these to be used in the medical field of both treatment and prevention, the structural and functional changes that occur need to be known in more detail. One way of achieving this could be via a study that follows a group of adolescents for an extended period of time, potentially into young or mid-adulthood, and regularly analyses the neurological changes that occur – by doing this, the longer term impacts of the initial alcohol use can be examined, allowing for this question in particular to be answered with a higher degree of accuracy. However, it is evident that though more primary sources of information are required, excessive alcohol consumption during this period can permanently alter and damage the development and function of the brain.

References

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

De Bellis, M.D; Clark, D.B.; Beers. S.R.; et al. 2000, Hippocampal volume in adolescent-onset alcohol use disorders. American Journal of psychiatry 157:734-744

De Bellis, M.D; Narasaimhan A; Thatcher D.L.; et al. 2005, Prefrontal cortex, thalamus, and cerebellar volumes in adolescents and young adults with adolescent-onset alcohol use disorders and comorbid mental disorders, 29:1590-1600

Duke Institute for Brain Sciences (2019). Michael De Bellis. Available at: https://dibs.duke.edu/scholars/michael-de-bellis

Hill, S.Y., and Shen, S. , 2002, Neurodevelopmental patterns of visual P3b in association with familial risk for alcohol dependence and childhood diagnosis. Biological Psychiatry 51:621-631

Hommer D.; Momenan, R.; Kaiser, E.; and Rawlings, R., 2001, Evidence for a gender-related effect of alcoholism on brain volumes. American Journal of Psychiatry 158:198-204

Nagel B.J.; Schweinsburg A.D.; Phan V, et al. 2005. Reduced hippocampal volume among adolescents with alcohol use disorders without psychiatric comorbidity, pages 139:181-190

NCBI – National Centre for Biotechnology Information (2000). Hippocampal volume in adolescent-onset disorders. Available at: https://www.ncbi.nlm.nih.gov/pubmed/10784466

NCBI – National Centre for Biotechnology Information (1993). P300 in heavy social drinkers: the effect of loreazepam. Available at: https://www.ncbi.nlm.nih.gov/pubmed/8397877?dopt=Abstract

Nichols, J.M., and Martin, 1993, F.P300 in heavy social drinkers: The effect of lorazepam. Alcohol 10:269-274

Photo Credits due to: Saeyon Nanthakumar

Saeyon Nanthakumar