Anohim M, Gibert Rahola J.

TA-ARCA Cádiz; Dpto. de Neurociencias, Facultad de Medicina, Universidad de Cádiz; CIBER del Área de Salud Mental, CIBERSAM.

INTRODUCTION

Teenage: the age of independence, new friends and self-discovering. It’s the period of “first times”: first moto, first love… and first parties. At 14 years old, 1 out 4 adolescents report to have drink alcohol in the past year. Moreover, half of the young between 12 and 15 years’ old who drank were engaged in binge drinking, which consists in drinking a lot in a small lapse of time1. So, if it is that frequent, why should it be a concern? Mostly because teenagers are more sensitive to binge drinking both socially and physically. More specifically, the impacts of binge drinking on their brain still in development (until 21 years old)2 could be catastrophic. Fortunately, science tries to find solution to this issue.

WHY SHOULD WE BE CONCERNED ABOUT BINGE-DRINKING IN ADOLESCENTS?

Teenagers are more susceptible to heavy-drink than adults, both because of social and biological factors. While drinking a lot is seen as abnormal in the 30’s, this behavior is highly encouraged in teenagers group and even in the 20’s3. When they were asked why they drink, 41% answered that they wanted to seem more sympathetic and fun while 14% thought it helped them flirting and meet new people4. We also see the emergence of the concept of pre-party, or botellón, in Spanish. In fact, in Spain, 21% of the youngsters had their first drink in those events. This practice is associated with the need of social acceptance and identification with pairs, which is an important issue in adolescence. As a matter of fact, having friends that drink is an important risk factor of underage drinking and it is part of the two more important screening questions for clinicians as suggested by National Institute on Alcohol Abuse and Alcoholism (NIAAA) in the United States1. To summarize, binge drinking is associated with social pressure in young people.

Teenagers’ brains also play them tricks that lead them to drink more. In fact, studies show that they are more susceptible than adults to feel the positive effects of alcohol5 (by overstimulation of amygdala and of recompense circuit) and less sensitive to immediate effects of sedation and motor incoordination6, symptoms that could have help them to stop drinking.

Moreover, less important amounts of alcohol are necessary to produce toxic effects in teenagers, both to the brain and to the rest of the body. While a binge drinking episode for males is defined as 5 drinks in less than 2 hours, we talk about 3 in the same lapse of time for the group of 9-13 years old, 4 for the 14-15 and 5 after 16 years old1. For females, we talk about 4 drinks in 2 hours for adults and 3 for 9 to 17 years old Additionally, the teen’s brain is particularly sensitive to alcohol effects. During adolescence, structures as hippocampus and prefrontal cortex are in development. Hippocampus is responsible of long term memory and attention, while prefrontal cortex regulates the executive functions (processing information, planning and abstract thinking). Prefrontal cortex is also responsible of the control of impulsivity. It results that alcohol induces an atrophy of hippocampus and a loss of grey matter in prefrontal cortex which affects all the functions led by these brain structures7. Furthermore, it has been shown that even just one episode of binge-drinking is responsible of neuroinflammation and production of oxidative stress8. Binge drinking has also been shown as ‘more predictive of neurodegeneration […] than lifetime duration of intake’9.

To summarize, binge drinking has to be addressed because it is a more dangerous way of consumption that chronic moderate-high taking, that is considered as a normal practice among teenagers and because it causes damages on the hippocampus, the prefrontal cortex and others areas of a brain in development.

WHAT CAN BE DONE TO PREVENT BRAIN INJURIES FROM BINGE-DRINKING?

What’s happening in the brain when we drink too much in a party? Alcohol induces activation of complex pathways, mediated by reactive oxygen species (ROS), cytokines, chemokines and oxidative enzymes that lead to inflammation, oxidation and neurodegeneration. Several studies have tried to find a treatment to prevent these damages and some of them will be resumed here.

Eating well and doing exercise

Some compounds of a healthy diet could actually prevent or reduce damage on brain caused by alcohol. A study published in 2016 has demonstrated that vitamin C is efficient at reducing ROS and at suppressing activation by alcohol of microglia and astrocytes (inflammatory cells specific to CNS) in 7 days old rats (with brain in development). Furthermore, it has been previously demonstrated that vitamin C protects from apoptotic cell death caused by alcohol. Although this study concentrated on the alcohol fetal syndrome, the results might apply also to teenagers, whose brain are also in development. Another compound of the diet that protects the brain from alcohol is fish oil. To be more precise, fish oil contains an omega-3 compound, the DHA (omega-3 docosahexanenoic acid) which is depleted by excessive alcohol consumption. When taken during an episode of binge drinking, DHA reduces the levels of phospholipase A2, induced by the ingestion of a high amount of alcohol. This results in less inflammation, as shown by lower levels of aquaporin 4 and less brain edema10. This study has been done in adult male rat models with binge-drinking. Therefore, it has his limits for being applied to the specificities of teenagers’ brains, even if it addresses a pattern of drinking more often employed by adolescents.

Doing exercise before binge drinking may reduce also impacts of alcohol on specific parts of brain, which are even more sensitive during the adolescence. In fact, a study made on female rats has shown than doing voluntary running before alcohol intake protects the hippocampus and the dentate gyrus (part of brain, which, in synergy with the hippocampus, helps to create and keep memories). Previously, we have seen that hippocampus is particularly fragile part of the teenager’s brain, as it matures during adolescence. Exercising ‘increases the proliferation, survival and neuronal differentiation of progenitor cells’9 in the hippocampus, which results in a better memory and learning skills.

Other possible treatments

Some molecules and drugs have also been investigated for preventing brain damage cause by ethanol.

Oleoylethanolamide (OEA) is a satiety factor produced by the small intestine, which has shown neuroprotective properties. When ingested in big quantities, ethanol activates the toll-like receptor TLR4 which causes inflammation an oxidative stress by the NF kappa B intracellular activation. This leads to neuronal damage and expression of the cytokine HMGB 1 which signals potential danger to brain. When taken before a binge, OEA reduces the expression of these three molecules (TLR4, NFkB and HMGB 1), therefore reducing inflammation and oxidative stress. These beneficial effects have been seen in the frontal cortex, which is also developing during adolescence. Consequently, the results of this study could apply to teens, even though the study has been performed on adult rats. Moreover, OEA is also efficient for diminishing the symptoms of depression caused by acute withdrawal11.

Glycine is a non-essential amino-acid, which has anti-oxidant properties. According to a study published in 2016, when administrated at the same as an acute alcohol consumption, glycine reduces expression of NFkB, of other products of oxidative cascade such as cyclooxygenase 2 (COX2) and of molecules of the inflammatory cascade, such as TNF-alpha. This amino-acid has therefore the capacity to reduce neuroinflammation and oxidative stress in young rats (7 days old, with brain in development)12. Even though the study has been made with the aim of preventing and treating alcohol fetal syndrome, teen brains are also in development.

CONCLUSION

During this essay, it has been shown that binge drinking is an important issue in adolescence, because it’s encouraged by pairs, who are also more important at this age. Moreover, brain particularities of the teens expose them to the possibility of drinking more without having the uncomfortable effects of alcohol. Consuming ethanol is also more dangerous for teenagers, because of the immaturity of their brain, exposing them to problems with memory and learning (hippocampus) and with executive functions and impulsivity control (prefrontal cortex).

Science has tried to find some remedies to brain damage caused by binge drinking. Among them, those that are applied to young brains, in development, are vitamin C and glycine. Exercising or taking glycine before alcohol intake have also been proven efficient in reducing brain damage of important regions, developing during adolescence, such as hippocampus and frontal cortex, respectively. Those studies were performed on adult rats, but because of their impacts of those important regions, their results can be extrapolated to youngsters. Fish oil has also shown interesting results to reduce alcohol damage on CNS, although it couldn’t be specifically applied to teenagers.

As it has been noted, there are not enough studies that address prevention of brain damages in teenagers specifically. It could be interesting to have more data on this subject, since is an important societal issue. On another hand, even if pharmacological and non-pharmacological solutions are proposed, none of the cited studies mentions that is acceptable to drink large amounts of alcohol in few time if a remedy is taken. Therefore, the best way of reducing that cerebral impact, is to prevent underage drinking and binge drinking in youngsters. In that state of mind, it is important to control very strictly the advertisements encouraging alcohol consumptions and to be sure none of them are addressed to minors. On that matter, there is still work to do. In fact, since 2005, children have been exposed more than 15 billion times to ads about alcohol that didn’t respect the rules imposed, estimates Craig Ross, researcher at the University of Boston, division of Public Health13,14,15.

REFERENCES

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