Summary: According to researchers, mixing high energy drinks with alcohol triggers changes in the teen brain similar to those experiences when taking cocaine.
Drinking highly caffeinated alcoholic beverages triggers changes in the adolescent brain similar to taking cocaine, and the consequences last into adulthood as an altered ability to deal with rewarding substances, according to a Purdue University study.
Richard van Rijn, an assistant professor of medicinal chemistry and molecular pharmacology, looked at the effects of highly caffeinated energy drinks and highly caffeinated alcohol in adolescent mice. These alcohol studies cannot be performed in adolescent humans, but changes seen in mouse brains with drugs of abuse have been shown to correlate to those in humans in many drug studies.
These energy drinks can contain as much as 10 times the caffeine as soda and are often marketed to adolescents. But little is known about the health effects of the drinks, especially when consumed with alcohol during adolescence.
Van Rijn and graduate student Meridith Robins published results in the journal Alcohol that showed adolescent mice given high-caffeine energy drinks were not more likely than a control group to drink more alcohol as adults.
But when those high levels of caffeine were mixed with alcohol and given to adolescent mice, they showed physical and neurochemical signs similar to mice given cocaine. Those results were published in the journal PLOS ONE.
“It seems the two substances together push them over a limit that causes changes in their behavior and changes the neurochemistry in their brains,” van Rijn said. “We’re clearly seeing effects of the combined drinks that we would not see if drinking one or the other.”
With repeated exposure to the caffeinated alcohol, those adolescent mice became increasingly more active, much like mice given cocaine. The researchers also detected increased levels of the protein ΔFosB, which is marker of long-term changes in neurochemistry, elevated in those abusing drugs such as cocaine or morphine.
“That’s one reason why it’s so difficult for drug users to quit because of these lasting changes in the brain,” van Rijn said.
Those same mice, as adults, showed a different preference or valuation of cocaine. Robins found that mice exposed to caffeinated alcohol during adolescence were less sensitive to the pleasurable effects of cocaine. While this sounds positive, it could mean that such a mouse would use more cocaine to get the same feeling as a control mouse.
“Mice that had been exposed to alcohol and caffeine were somewhat numb to the rewarding effects of cocaine as adults,” van Rijn said. “Mice that were exposed to highly caffeinated alcoholic drinks later found cocaine wasn’t as pleasurable. They may then use more cocaine to get the same effect.”
To test that theory, Robins investigated if mice exposed to caffeinated alcohol during adolescence would consume higher amounts of a similarly pleasurable substance – saccharine, an artificial sweetener. They predicted that if the mice exhibited a numbed sense of reward, they would consume more saccharine. They found that the caffeine/alcohol-exposed mice drank significantly more saccharine than mice exposed to water during adolescence, confirming that the caffeine/alcohol-exposed mice must have had a chemical change in the brain.
“Their brains have been changed in such a way that they are more likely to abuse natural or pleasurable substances as adults,” van Rijn said.
Van Rijn plans to continue studying the effects of legal, available psychostimulatory substances that may be harmful to adolescent brains. His next project involves investigating ethylphenidate, a drug similar to methylphenidate, the drug used for attention deficit disorder and most commonly known as Ritalin. The latter requires a prescription, while the former can be purchased without one, often online. His research group also works on finding new treatments for alcohol use disorder.
About this neuroscience research article
Funding: Van Rijn’s research is supported by the National Institute on Alcohol Abuse and Alcoholism, the Alcoholic Beverage Medical Research Foundation/Foundation for Alcohol Research and the Ralph W. and Grace M. Showalter Research Trust.
Source: Amy Patterson Neubert – Purdue Image Source: NeuroscienceNews.com image is in the public domain. Original Research:Abstract for “Adolescent intake of caffeinated energy drinks does not affect adult alcohol consumption in C57BL/6 and BALB/c mice” by Meridith T. Robins, Julia N. DeFriel, Richard M. van Rijn in Alcohol. Published online October 2016 doi:10.1016/j.alcohol.2016.05.001
Full open access research for “Unique Behavioral and Neurochemical Effects Induced by Repeated Adolescent Consumption of Caffeine-Mixed Alcohol in C57BL/6 Mice” byMeridith T. Robins, Julie Lu, Richard M. van Rijn in PLOS ONE. Published online July 5 2016 doi:10.1371/journal.pone.0158189
Cite This NeuroscienceNews.com Article
[cbtabs][cbtab title=”MLA”]Purdue “Mixing Energy Drinks and Alcohol May Affect Adolescent Brains Like Cocaine.” NeuroscienceNews. NeuroscienceNews, 24 October 2016. <https://neurosciencenews.com/alcohol-energ-drink-neurodevelopment-5337/>.[/cbtab][cbtab title=”APA”]Purdue (2016, October 24). Mixing Energy Drinks and Alcohol May Affect Adolescent Brains Like Cocaine. NeuroscienceNew. Retrieved October 24, 2016 from https://neurosciencenews.com/alcohol-energ-drink-neurodevelopment-5337/[/cbtab][cbtab title=”Chicago”]Purdue “Mixing Energy Drinks and Alcohol May Affect Adolescent Brains Like Cocaine.” https://neurosciencenews.com/alcohol-energ-drink-neurodevelopment-5337/ (accessed October 24, 2016).[/cbtab][/cbtabs]
Adolescent intake of caffeinated energy drinks does not affect adult alcohol consumption in C57BL/6 and BALB/c mice
The rise in marketing and mass consumption of energy drink products by adolescents poses a largely unknown risk on adolescent development and drug reward. Yet, with increasing reports of acute health issues present in young adults who ingest large quantities of energy drinks alone or in combination with alcohol, the need to elucidate these potential risks is pressing. Energy drinks contain high levels of caffeine and sucrose; therefore, exposure to energy drinks may lead to changes in drug-related behaviors since caffeine and sucrose consumption activates similar brain pathways engaged by substances of abuse. With a recent study observing that adolescent caffeine consumption increased cocaine sensitivity, we sought to investigate how prolonged energy drink exposure in adolescence alters alcohol use and preference in adulthood. To do so, we utilized three different energy drink exposure paradigms and two strains of male mice (C57BL/6 and BALB/c) to monitor the effect of caffeine exposure via energy drinks in adolescence on adult alcohol intake. These paradigms included two models of volitional consumption of energy drinks or energy drink-like substances and one model of forced consumption of sucrose solutions with different caffeine concentrations. Following adolescent exposure to these solutions, alcohol intake was monitored in a limited-access, two-bottle choice between water and increasing concentrations of alcohol during adulthood. In none of the three models or two strains of mice did we observe that adolescent ‘energy drink’ consumption or exposure was correlated with changes in adult alcohol intake or preference. While our current preclinical results suggest that exposure to large amounts of caffeine does not alter future alcohol intake, differences in caffeine metabolism between mice and humans need to be considered before translating these results to humans.
“Adolescent intake of caffeinated energy drinks does not affect adult alcohol consumption in C57BL/6 and BALB/c mice” by Meridith T. Robins, Julia N. DeFriel, Richard M. van Rijn in Alcohol. Published online October3 2016 doi:10.1016/j.alcohol.2016.05.001
Unique Behavioral and Neurochemical Effects Induced by Repeated Adolescent Consumption of Caffeine-Mixed Alcohol in C57BL/6 Mice
The number of highly caffeinated products has increased dramatically in the past few years. Among these products, highly caffeinated energy drinks are the most heavily advertised and purchased, which has resulted in increased incidences of co-consumption of energy drinks with alcohol. Despite the growing number of adolescents and young adults reporting caffeine-mixed alcohol use, knowledge of the potential consequences associated with co-consumption has been limited to survey-based results and in-laboratory human behavioral testing. Here, we investigate the effect of repeated adolescent (post-natal days P35-61) exposure to caffeine-mixed alcohol in C57BL/6 mice on common drug-related behaviors such as locomotor sensitivity, drug reward and cross-sensitivity, and natural reward. To determine changes in neurological activity resulting from adolescent exposure, we monitored changes in expression of the transcription factor ΔFosB in the dopaminergic reward pathway as a sign of long-term increases in neuronal activity. Repeated adolescent exposure to caffeine-mixed alcohol exposure induced significant locomotor sensitization, desensitized cocaine conditioned place preference, decreased cocaine locomotor cross-sensitivity, and increased natural reward consumption. We also observed increased accumulation of ΔFosB in the nucleus accumbens following repeated adolescent caffeine-mixed alcohol exposure compared to alcohol or caffeine alone. Using our exposure model, we found that repeated exposure to caffeine-mixed alcohol during adolescence causes unique behavioral and neurochemical effects not observed in mice exposed to caffeine or alcohol alone. Based on similar findings for different substances of abuse, it is possible that repeated exposure to caffeine-mixed alcohol during adolescence could potentially alter or escalate future substance abuse as means to compensate for these behavioral and neurochemical alterations.
“Unique Behavioral and Neurochemical Effects Induced by Repeated Adolescent Consumption of Caffeine-Mixed Alcohol in C57BL/6 Mice” byMeridith T. Robins, Julie Lu, Richard M. van Rijn in PLOS ONE. Published online July 5 2016 doi:10.1371/journal.pone.0158189