Effects of adolescent alcohol use on brain maturation in the hippocampus and
prefrontal cortex and associated neurocognitive performance deficits: a
review of the literature
1. INTRODUCTION
The issue of adolescent alcohol use has slowly become a more prominent issue, with
younger and younger populations consuming alcohol (Zeigler et al. 2005). Some studies suggest
that now children have their first alcoholic drink as early as age twelve (Zeigler et al. 2005) and
nearly 1 in 4 youths qualify for a substance use disorder before age twenty (Squeglia et al. 2009).
Adolescent use of alcohol is widespread, as suggested by the Monitoring the Future Study, which
found that 72.3% of high school seniors report having used alcohol at some point in their life
(Johnston et al. 2009). Several researchers have delved into determining the effects of using
alcohol before brain maturity is complete. Research suggests that adolescent use of alcohol
results in significant neurocognitive development and performance deficits, specifically in the
hippocampus, prefrontal cortex, and working memory systems.
It has been shown that heavy use in adults with alcohol dependence disorders correlates
with brain dysfunctions, but only recently has research begun to explore the same possibility in
adolescents. Adolescence, here defined as ages 12 to 20, is a vital neurodevelopmental period,
during which much brain maturation occurs (Guerri and Pascual 2010). The effects of alcohol
use during this critical developmental period could prove detrimental to the neurocognitive
function in adolescents and could result in significant brain atrophy, coined neurodevelopmental
dysmaturation (Clark et al. 2008)
2. METHODS
A PubMed search was done using the key words “adolescence”, “alcohol”, “brain
development”, “brain maturation”, and “neurocognition”. Articles were further qualified by their
publication date, with years ranging from 2000-2010, and language, allowing for articles in
English only. Articles were first selected based on their relevance to adolescent alcohol use and
its effects on neurological development and maturation. Articles that either explained either the
processes of neuromaturation or the effects of adolescent alcohol use on those processes were
also selected.
3. RESULTS
3.1. Key Terminology
1. Gray Matter – The brain’s neurons and their dendrites (National Institute of Mental Health
2010).
2. White Matter – The long fibers that form the long-distance connections between the brain
regions (National Institute of Mental Health 2010).
3. Heavy Drinker – One who consumed 5+ drinks on the same occasion on at least 5 different
occasions in the past 30 days (Zeigler et al. 2005).
4. Functional Magnetic Resonance Imaging (fMRI) – Non-invasive method used to quantify
substrates in the brain. It reflects changes in the chemical composition of brain structures during
specific neuroperformance tests (Squeglia et al. 2009).
5. Blood Oxygen Level Dependent (BOLD) – Measures oxygen distribution in the brain to
determine areas of increased activation during specific neuroperformance tests (Squeglia et al.
2009).
6. Working Memory – Short-term memory, or a system to store and manage the information
required to complete cognitive tasks. (Medicine Net 1998)
7. Diffusion Tensor Imaging (DTI) – Examines the diffusion of water molecules in the white
matter tissue in the brain (Squeglia et al. 2009).
3.2. Typical Adolescent Brain Development and Maturation
Many different neuromaturation processes actually occur during adolescence. Guerri and
Pascual name 3 main processes: proliferation, pruning, and myelination (2010). Proliferation
refers to the processes that create new connections within the brain. Maximum brain size is
reached before adolescence, but new connections are made throughout adolescence. Pruning
refers to gray matter maturation. Despite proliferation in the brain, many more connections are
destroyed through pruning resulting in a net reduction of gray matter volume. This process is
especially sensitive to environmental influences and can make the brain much more elastic (Witt
2010). Myelination speeds up neural transmission by further myelinating axons, or adding fatty
tissue surrounding a neuron (Guerri and Pascual 2010). This myelination is generally assumed
to increase the speed of information processing within the brain. An increase in white matter
volume is directly associated with this process.
The brain’s efficiency is significantly improved through pruning and myelination. The
hippocampus is mainly responsible for memory. The prefrontal cortex is known for its role in
planning, organizing, and decision-making. Both of these brain regions quickly develop during
adolescence (Zeigler et al. 2005). The volume of the prefrontal cortex decreases as one moves
from adolescence into young adulthood because of pruning (Guerri and Pascual 2010).
3.3. Neurodevelopmental Dysmaturation
3.3.a. Hippocampus
The gray matter volume in the hippocampus has been shown to negatively correlate with
adolescent alcohol use (Zeigler et al. 2005). Magnetic resonance imaging (MRI) techniques
were commonly used to assess these deficiencies. Heavy adolescent drinkers showed the
greatest discrepancy from non-using adolescent controls. Atrophy was determined to be
particularly significant in the left hippocampus. In a study, the non-using participants who had a
greater hippocampal volume on the right side than on the left showed a greater verbal learning
ability (Squeglia et al. 2009). Although many alcohol-using participants also showed a greater
right than left hippocampal volume, this superior verbal learning was absent in the ‘using’
groups. This hippocampal defect can be attributed to inflammation and the creation of fatty acid
ethyl esters that are produced in the brain (Clark et al. 2008). These esters are created in
response to the consumption of ethanol, and have been known to be harmful to the hippocampus
(Mechtcheriakov et al. 2007).
3.3.b. Prefrontal Cortex
Much of the synaptic pruning and myelination during adolescence occurs in the
prefrontal cortex, aimed at increasing the efficiency of the brain (Guerri and Pascual 2010). A
significantly smaller prefrontal cortex volume has been observed in heavy drinkers compared to
non-users, especially in females (Squeglia et al. 2009), although it is disputed the extent to which
females are additionally affected (Mechtcheriakov et al. 2007). The prefrontal cortex is
responsible for personality traits, planning, goal-directed behaviors and impulse control (Zeigler
et al. 2005). The negative consequences on this critical part of the brain can explain many
deficits associated with alcohol use because reasoning abilities are underdeveloped, which
further increases the likelihood that an adolescent will consume and abuse alcohol (Squeglia et
al. 2009).
3.4 Spatial Workming Memory (SWM) Performance Deficits
Squeglia et al. (2009) found that SWM deficits existed between participants who had
been heavy drinkers for at least one year and light drinkers. This discrepancy was found using
neuroimaging techniques of fMRI and BOLD. The fMRI and BOLD tests revealed that brain
structure activation was lacking among heavy alcohol users in the frontal and parietal regions of
the brain, which includes both the hippocampus and prefrontal cortex (Zeigler et al. 2005). This
shortfall was more prominent in the right hemisphere of the brain. A positive correlation was
also found between alcohol consumption and cognitive performance deficits (Squeglia et al.
2009). A study was conducted using adolescents who had engaged in 5 or more years of heavy
alcohol use (Squeglia et al. 2009). These adolescents showed even greater performance deficits
in measuring SWM, furthering the belief that increase in alcohol use results in greater deficits.
4. CONCLUSION
The vast majority of the published research suggests that adolescent alcohol use results in
brain dysmaturation by altering the many brain maturation processes that occur during
adolescence. These specific brain atrophies result in significant performance deficits that should
not be taken lightly. More research should be conducted to determine specific ages, not just age
ranges, during which the adolescent brain is most vulnerable to the harmful effects of alcohol
consumption. Current legislation states the legal drinking age to be 21, however, this age may
need to be modified upon the results of the further research to protect the integrity of the
adolescents’ brains. In addition, more funding should be put into education of adolescents, and
their parents, about the danger of underage alcohol consumption because most people
underestimate its devastating effects.
Further research should focus on establishing a causal link between brain atrophy and
adolescent alcohol use. DTI should be used in combination with fMRI to detect the brain’s
white matter tissue organization and volume differences in comparison to its functional activity
in both using and non-using adolescents. DTI is a more sensitive alternative to a traditional MRI
and better defines the true brain volumes, making it a superior alternative. However, DTI only
provides information on white matter, so a MRI is still necessary for gray matter tissue
organization. Several longitudinal studies must be conducted to look at the possibility that the
brain differences are an innate quality that increases the likelihood of alcohol use. The
dysmaturation of the prefrontal cortex would suggest decreased reasoning and inhibition abilities
and could result in increased alcohol use. Future research studies should merge the ideas of
biological and environmental determinants as foundations for either increased alcohol use or
brain dysmaturaion, respectively.
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