Researchers from Purdue University (West Lafayette, IN, USA) have observed that consumption of highly caffeinated alcoholic beverages elicits alterations in the adolescent brain, activating similar brain pathways engaged by substances of abuse such as cocaine.
The study, published in PLoS ONE, investigated prolonged caffeine-mixed alcohol exposure in adolescent C57BL/6 mice models of common drug-related behaviors such as locomotor sensitivity, drug reward, cross-sensitivity and natural reward following previous research that demonstrated adolescent caffeine consumption may increase cocaine sensitivity.
“It seems the two substances together push them over a limit that causes changes in their behavior and changes the neurochemistry in their brains,” commented author Richard van Rijn (Purdue University). “We’re clearly seeing effects of the combined drinks that we would not see if drinking one or the other.”
To investigate alterations in neurological activity as a result of adolescent caffeine-mixed alcohol exposure, the team monitored changes in expression of the transcription factor ΔFosB in the dopaminergic pathway to measure signs of long-term increases in neuronal activity.
The team observed that repeated exposure to caffeine-mixed alcohol induced significant locomotor sensitization, desensitized cocaine conditioned place preference, decreased cocaine locomotor cross-sensitivity and increased natural reward consumption in adolescent C57BL/6 mice. While this sounds positive, it could result in behavior whereby more cocaine will be used to attain the desired effect.
“Mice that had been exposed to alcohol and caffeine were somewhat numb to the rewarding effects of cocaine as adults,” van Rijn explained. “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 further investigate if the mice exposed to caffeine-mixed alcohol during adolescence would consume larger amounts of pleasurable substances, the team utilized saccharine, an artificial sweetener. They observed that caffeine-mixed alcohol-exposed mice consumed significantly more saccharine than control mice.
Additionally, utilizing the exposure model the team observed increased accumulation of ΔFosB in the nucleus accumbens and unique behavioral and neurochemical effects following prolonged adolescent caffeine-mixed alcohol exposure when compared to alcohol or caffeine alone.
“Their brains have been changed in such a way that they are more likely to abuse natural or pleasurable substances as adults,” van Rijn elaborated.
Based on previous research for different substances of abuse, these findings may indicate 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. However, despite the preclinical findings, the difference in caffeine and alcohol metabolism between mice and humans needs to be considered before translating results to humans.
Sources: Robins MT, DeFriel JN, van Rijn RM. Unique behavioural and Neurochemical effects induced by repeated adolescent consumption of caffeine-mixed alcohol in C57BL/6 mice. PLos ONE doi:10.1371/journal.pone.0158189 (2016) (Epub ahead of print); www.purdue.edu/newsroom/releases/2016/Q4/mixing-energy-drinks,-alcohol-may-affect-adolescent-brains-like-cocaine.html