10. The adolescent brain and alcohol

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A useful introductory video: The Teenage Brain and Addiction – YouTube

According to Britannica.com, adolescence is defined the traditional phase of growth and development between childhood and adulthood. The World Health Organization (WHO) defines an adolescent as any person between ages 10 and 19. This age range falls within WHO’s definition of young people, which refers to individuals between ages 10 and 24.

It is during this time that the individual’s brain undergoes gradual changes, first by increasing grey matter (nerve cell bodies), and then, later in adolescence, a pruning process of grey matter reduction, accompanied by an increase in white matter volume and integrity with continued myelination of axons, allowing for more efficient communication between brain regions.

At the same time, the sensitivity of the adolescent brain to stimuli because of a gradual change in distribution of neurotransmitter receptors. During adolescence, the brain is rich in receptors for dopamine, the neurotransmitter involved in marking pleasurable events. Meanwhile, the adolescent brain has a relatively low concentration of receptors for GABA, which is the principal inhibitory neurotransmitter. The gradual reduction of dopamine receptors and concomitant increase in GABA receptors will come later, with maturity.

The net result of these distributions of receptors is that the adolescent will show heightened reward sensitivity, sensation seeking and impulsive action, while at the same time, will show diminished self-control to inhibit emotions and behaviors.

Global prevalence of adolescent alcohol use

The average age of initiation for alcohol use among US and Australian adolescents is 15 years, while across Europe, most adolescents begin drinking between ages 12 and 16.

The initiation of drinking, particularly binge drinking during adolescence, can be damaging, and the damage that is incurred can be very long-lasting. The following chart, adapted from Table 1 of Lees et. al. (2020), summarizes the consequences of adolescent alcohol use in humans:

Decreases in:

  1. Immediate recall (short-term memory)
  2. Delayed retention, recall (long-term memory)
  3. Learning
  4. Visuospatial function
  5. Working memory
  6. General cognitive functioning
  7. Verbal memory
  8. Executive functioning
  9. Semanic clustering
  10. Reading skills
  11. Grey matter volume, particularly frontal, temporal
  12. White matter growth
  13. White matter integrity

Heavy drinking adolescents showed less baseline brain activation in frontal and parietal regions during a visual working memory and inhibition task when compared to controls. This suggests that youth who initiate heavy drinking may require more executive cognitive control to perform at the same level as non-users.

Increases in:

  1. Impulsivity
  2. Cerebrospinal fluid volume in the cerebellum

Cognitive and neural functioning followed alcohol remittance (discontinuation)

While there is some improvement, there are some studies which show that impairment can be long-lasting. For example, a 10-year study found remitted you, who had previously met criteria for an alcohol use disorder, performed similarly to youth with persistent disorders on tasks measuring visuospatial functioning and language abilities.

Adolescent alcohol effects in animals

Experiments with animals, particularly with rodents, allows scientists to understand, in greater detail, the differences in responses between adolescent and adult animals.

For example, adolescent animals are less sensitive than adults to many of the intoxicating alcohol effects that serve as cues to stop drinking, such as alcohol’s motor-impairing, sedative, social-inhibiting and hangover-inducing effects. At the same time, adolescent animals are MORE sensitive to than adults to desirable consequences of low levels of alcohol use, including social facilitation and rewarding effects.

Lees, B.; Meredith, L.R.; Kirkland, A.E.; Bryant, B.E.; Squeglia, L.M. (2020). Effect of alcohol use on the adolescent brain and behavior. Pharmacol Biochem Behav. 2020 May; 192: 172906. doi:10.1016/j.pbb.2020.172906.