Elio Acquas
Laura Dazzi
Mercè Correa
John D. Salamone
Valentina Bassareo- 1Department of Life and Environmental Sciences, University of Cagliari, Monserrato, Italy
- 2Department of Psychobiology, University Jaume I, Castelló, Spain
- 3Department of Psychological Sciences, University of Connecticut, Storrs, CT, United States
- 4Department of Biomedical Sciences, University of Cagliari, Monserrato, Italy
Editorial on the Research Topic
Alcohol and energy drinks: is this a really good mix?
From the first appearance of Red Bull (RB) on the market in 1987 (Reissig et al., 2009), energy drinks (EDs) have become increasingly popular among adolescents and young adults, and their consumption has increased to an alarming extent. There are some well-known adverse effects on the cardiovascular and cerebrovascular systems, such as cardiomyopathies, atrial and ventricular arrhythmias, myocardial infarctions, cardiac death (Mangi et al., 2017; Ehlers et al., 2019; Cao et al., 2021; Piccioni et al., 2021) and cardiovascular and cerebrovascular modifications (Costa et al., 2023). Other effects have also been reported including excitability, irritability, anxiety, insomnia, headache, malaise, nausea/vomiting and abdominal pain (Wolk et al., 2012; Nadeem et al., 2021; Khouja et al., 2022). Moreover, it has been described that the intake of great amounts of EDs produces convulsions, cerebral hemorrhage, psychosis, suicidal thoughts, and acute liver and renal damage (Hernandez-Huerta et al., 2017; Kim et al., 2018; Kelsey et al., 2019).
The articles collected in this Frontiers Research Topic provide an overview of the results of recent studies on the effects of EDs in rodents, the role of some of the common ingredients of EDs on alcohol-induced behaviors, the side effects of the use of alcohol mixed with ED (AMED) for the developing brain of adolescents and the medical and socio-legal standpoints on this EDs association.
Petribu et al. analyzed several studies reporting that the acute or chronic AMED consumption, enhanced the alcohol intake and his motivational value, dose-dependently stimulated locomotion, and deteriorated movements capability. AMED intake time-dependently reduced anxiety, and a wide variety of effects on memory have been reported. The acute administration of AMED did not modify alcohol metabolism, but after its chronic assumption, blood alcohol concentrations were higher or lower than those of the alcohol-only group depending on the paradigm used. A comparable range of effects has been described about metabolic dysfunction. AMED intake produced an increase of pro-inflammatory cytokines, created oxidative stress and lipid peroxidation, but also in this case the results obtained depend on the protocol used. Briefly, AMED produces different outcomes depending on the amount of alcohol and EDs and the age, sex, and line of animals used.
Unfortunately, different studies have been conducted on EDs that contain several substances, but fewer studies have focused on the individual ingredients at well-established concentrations. This is a critical point that may preclude the identification of any potential interaction between components. Thus, while the association between caffeine, one of the principal ingredients of EDs, and alcohol has been previously analyzed, the associations with other active ingredients such as taurine, glucuronolactone, sucrose, B vitamins, are less studied. Sefen et al. addressed this issue and reported that the stimulatory properties of caffeine reduce the sedative effects of alcohol, making individuals more inclined to consume higher amount of alcohol -as they do not perceive the feeling of drunkness- and promoting risk-taking behavior. The increase of AMED drinking can be explained through activation on adenosine A2A receptors, which reduces alcohol intake (Houchi et al., 2008). Moreover, caffeine-induced inhibition of this receptor may contribute to enhanced alcohol consumption (Ferré, 2010). As reported by Cadoni and Peana, preclinical studies using rats, described that caffeine can promote alcohol self-administration (Kunin et al., 2000; Arolfo et al., 2004). Moreover, Sefen et al. indicated that caffeine significantly prevented alcohol-elicited conditioned-place preference and the acquisition of alcohol-elicited conditioned-place aversion (Porru et al., 2020). This seems to suggest that caffeine may have a protective effect on the abuse potential of alcohol. However, Cadoni and Peana referred that Vargiu et al. (2021) found that chronic consumption of RB in adolescent rats potentiates dopamine transmission in the nucleus accumbens shell by a nonadaptive mechanism, like drugs of abuse. The repeated stimulation of dopamine in the nucleus accumbens shell after repetitive EDs consumption can underlie the gateway effect toward the use of different substances of abuse.
Another relevant component of EDs is taurine, the most abundant intracellular amino acid in humans. Taurine does not affect levels of dopamine (Wu et al., 2017), but this compound can modify dopaminergic transmission in brain circuits involved in the regulation of drug intake (Adermark et al., 2011; Chen et al., 2018). Pulcinelli et al. (2020) reported that chronic administration of taurine enhances the voluntary intake of alcohol; they hypothesized that this result could be explained by an anxiolytic effect of taurine obtained by an interaction between GABA and dopamine systems.
The amount of B2, B3, B5, B6, and B12 vitamins in several EDs is higher than the recommended daily doses (Jagim et al., 2022), and the only evidence referred by Tarragon suggests that a proper intake of vitamins with the diet might limit the adverse consequences of alcohol on B-vitamin metabolism (Miyazaki et al., 2012).
An important aspect highlighted by Cadoni and Peana is the serious concern on the negative effects of EDs intake on the processes of neurodevelopment in the brain of adolescents that are the main consumers of these beverages (Seifert et al., 2011; Gallimberti et al., 2013).
Purines are involved in the refinement of several processes during the development of the brain, in particular in its growing architecture (Rodrigues et al., 2019). Acting on A1 receptors in different brain areas (hippocampus and cortex), adenosine modulates immature synapses (Jeong et al., 2003; Kerr et al., 2013; Burnstock and Dale, 2015). Accordingly, an excessive intake of caffeine can interfere with the purinergic transmission resulting in altered brain development that can lead to alterations of different brain functions (Silva et al., 2013; Al-Basher et al., 2018; Serdar et al., 2019; Zhang et al., 2020, 2022; Christensen et al., 2021; Agarwal et al., 2022). In addition, Brown et al. (2020) described that an excessive intake of taurine by adolescents or young adults can impair learning and memory function. The suggested mechanism for many alterations in several brain functions is an impairment of oligodendrocytes and neurons development, and of the harmonic process of synaptic pruning and formation of new synapses during the final cortical maturation (Serdar et al., 2019).
Finally, the original report by Sefen et al. on the regulation of AMED around the world can help the scientific community and influence public opinion and regulatory agencies to reflect on the need to regulate the sale and the consumption of EDs and AMED. In this regard, we foresee that the articles presented in this Research Topic provide a view of current preclinical and clinical studies in the field and allow new insights into the effects of AMED consumption on human health.
Author contributions
VB wrote the article. EA, LD, MC, and JS critically revised and approved the final version of the manuscript. All authors contributed to the article and approved the submitted version.
Funding
This work was supported by grants from Fondazione Banco di Sardegna (CUP F74I19000970007/2018).
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
References
Adermark, L., Clarke, R. B., Olsson, T., Hansson, E., Söderpalm, B., Ericson, M., et al. (2011). Implications for glycine receptors and astrocytes in ethanol-induced elevation of dopamine levels in the nucleus accumbens. Addict. Biol. 16, 43–54. doi: 10.1111/j.1369-201000206.x
Agarwal, K., Manza, P., Tejeda, H. A., Courville, A. B., Volkow, N. D., Joseph, P. V., et al. (2022). Prenatal caffeine exposure is linked to elevated sugar intake and bmi, altered reward sensitivity, and aberrant insular thickness in adolescents: an ABCD investigation. Nutrients 14, 4643. doi: 10.3390/nu14214643
Al-Basher, G. I., Aljabal, H., Almeer, R. S., Allam, A. A., and Mahmoud, A. M. (2018). Perinatal exposure to energy drink induces oxidative damage in the liver, kidney and brain, and behavioral alterations in mice offspring. Biomed. Pharmacother. 102, 798–811. doi: 10.1016/j.biopha.03139
Arolfo, M., Yao, L., Gordon, A. S., Diamond, I., and Janak, P. H. (2004). Ethanol operant self-administration in rats is regulated by adenosine A2 receptors. Alcohol Clin. Exp. Res. 28, 1308–1316.
Brown, J., Villalona, Y., Weimer, J., Ludwig, C. P., Hays, B. T., Massie, L., et al. (2020). Supplemental taurine during adolescence and early adulthood has sex-specific effects on cognition, behavior and neurotransmitter levels in C57BL/6J mice dependent on exposure window. Neurotoxicol. Teratol. 79, 106883. doi: 10.1016/j.ntt.2020.106883
Burnstock, G., and Dale, N. (2015). Purinergic signalling during development and ageing. Purinergic Signal. 11, 277–305. doi: 10.1007/s11302-015-9452-9
Cao, D. X., Maiton, K., Nasir, J. M., Estes, N. A. M., and Shah, S. A. (2021). Energy drink-associated electrophysiological and ischemic abnormalities: a narrative review. Front. Cardiovasc. Med. 8, 679105. doi: 10.3389/fcvm.2021.679105
Chen, V. C., Chiu, C. C., Chen, L. J., Hsu, T. C., and Tzang, B. S. (2018). (2018). Effects of taurine on striatal dopamine transporter expression and dopamine uptake in SHR rats. Behav. Brain. Res. 348, 219–226. doi: 10.1016/j.bbr.04031
Christensen, Z. P., Freedman, E. G., and Foxe, J. J. (2021). Caffeine exposure in utero is associated with structural brain alterations and deleterious neurocognitive outcomes in 9–10 year old children. Neuropharmacology 186, 108479. doi: 10.1016/j.neuropharm.2021.108479
Costa, R., Rocha, C., and Santos, H. (2023). Cardiovascular and cerebrovascular response to redbull® energy drink intake in young Adults. Anatol J Cardiol 27, 19–25. doi: 10.14744/AnatolJCardiol.2022.2315
Ehlers, A., Marakis, G., Lampen, A., and Hirsch-Ernst, K. I. (2019). (2019). Risk assessment of energy drinks with focus on cardiovascular parameters and energy drink consumption in Europe. Food Chem. Toxicol. 130, 109-121. doi: 10.1016/j.fct.05028
Ferré, S. (2010). Role of the central ascending neurotransmitter systems in the psychostimulant effects of caffeine. J Alzheimers Dis. 20, S35–49. doi: 10.3233/JAD-2010-1400
Gallimberti, L., Buja, A., Chindamo, S., Vinelli, A., Lazzarin, G., Terraneo, A., et al. (2013). Energy drink consumption in children and early adolescents. Eur. J. Pediatr. 172, 1335–40. doi: 10.1007/s00431-013-2036-1
Hernandez-Huerta, D., Martin-Larregola, M., Gomez-Arnau, J., Correas-Lauffer, J., and Dolengevich-Segal, H. (2017). Psychopathology related to energy drinks: a psychosis case report. Case Rep. Psychiatry 2017, 5094608. doi: 10.1155/2017/5094608
Houchi, H., Warnault, V., Barbier, E., Dubois, C., Pierrefiche, O., Ledent, C., et al. (2008). Involvement of A2A receptors in anxiolytic, locomotor, motivational properties of alcohol in mice. Genes Brain Behav. 7, 887–898. doi: 10.1111/j.1601-183x.2008.00427.x
Jagim, A. R., Harty, P. S., Barakat, A. R., Erickson, J. L., Carvalho, V., Khurelbaatar, C., et al. and Kerksick, C.M. (2022) “Prevalence amounts of common ingredients found in energy drinks shots”, nutrients. Multidiscip. Dig. Publ. Inst. (MDPI) 14, 314. doi: 10.3390./NU14020314.
Jeong, H. J., Jang, I. S., Nabekura, J., and Akaike, N. (2003). Adenosine A1 receptor-mediated presynaptic inhibition of GABAergic transmission in immature rat hippocampal CA1 neurons. J. Neurophysiol. 89, 1214–1222. doi: 10.1152/jn.00516.2002
Kelsey, D., Berry, A. J., Swain, R. A., and Lorenz, S. (2019). A case of psychosis and renal failure associated with excessive energy drink consumption. Case Rep. Psychiatry 24, 3954161. doi: 10.1155/2019/3954161
Kerr, M. I., Wall, M. J., and Richardson, M. J. (2013). Adenosine A1 receptor activation mediates the developmental shift at layer 5 pyramidal cell synapses and is a determinant of mature synaptic strength. J. Physiol. 591, 3371–80. doi: 10.1113/jphysiol.2012.244392
Khouja, C., Kneale, D., Brunton, G., Raine, G., Stansfield, C., Sowden, A., et al. (2022). Consumption and effects of caffeinated energy drinks in young people: an overview of systematic reviews and secondary analysis of UK data to inform policy. BMJ Open 12, e047746. doi: 10.1136/bmjopen-2020-047746
Kim, J. S., Kim, K., and Seo, Y. (2018). Associations between Korean adolescents' energy drink consumption and suicidal ideation and attempts. Arch. Psychiatr. Nurs. 32, 331–336. doi: 10.1016/j.apnu.2017.11.006
Kunin, D., Gaskin, S., Rogan, F., Smith, B., and Amit, Z. (2000). Caffeine promotes ethanol drinking in rats: examination using a limited-access free choice paradigm. Alcohol 21, 271–277. doi: 10.1016/s0741-8329(00)00101-4
Mangi, M. A., Rehman, H., Rafique, M., and Illovsky, M. (2017). Energy drinks and the risk of cardiovascular disease: a review of current literature. Cureus 9, e1322. doi: 10.7759/cureus.1322
Miyazaki, A., Sano, M., Fukuwatari, T., and Shibata, K. (2012). Effects of ethanol consumption on the B-group vitamin contents of liver, blood and urine in rats. Br. J. Nutri. 108, 1034–1041. doi: 10.1017/S0007114511006192
Nadeem, I. M., Shanmugaraj, A., Sakha, S., Horner, N. S., Ayeni, O. R., Khan, M., et al. (2021). Energy drinks and their adverse health effects: a systematic review and meta-analysis. Sports Health 13, 265–277. doi: 10.1177/1941738120949181
Piccioni, A., Covino, M., Zanza, C., Longhitano, Y., Tullo, G., Bonadia, N., et al. (2021). Energy drinks: a narrative review of their physiological and pathological effects. Intern. Med. J. 51, 636–646. doi: 10.1111/imj.14881
Porru, S., Maccioni, R., Bassareo, V., Peana, A. T., Salamone, J. D., Correa, M., et al. (2020). Effects of caffeine on ethanol-elicited place preference, place aversion and ERK phosphorylation in CD-1 mice. J. Psychopharmacol. 34, 1357–1370. doi: 10.1177/0269881120965892
Pulcinelli, R. R., Paula, de., Nietiedt, L. F., Bandiera, N. A., Hansen, S., Izolan, A. W., et al. (2020). R. (2020). Taurine enhances voluntary alcohol intake and promotes anxiolytic-like behaviors in rats. Alcohol 88, 55–63. doi: 10.1016/j.alcohol.07004
Reissig, C. J., Strain, E. C., and Griffiths, R. R. (2009). Caffeinated energy drinks-a growing problem. Drug Alcohol. Depend. 99, 1–10. doi: 10.1016/j.drugalcdep.2008.08.001
Rodrigues, R. J., Marques, J. M., and Cunha, R. A. (2019). Purinergic signalling and brain development. Semin. Cell. Dev. Biol. 95, 34–41. doi: 10.1016/j.semcdb.12001
Seifert, S. M., Schaechter, J. L., Hershorin, E. R., and Lipshultz, S. E. (2011). Health effects of energy drinks on children, adolescents, and young adults. Pediatrics 127, 511e.28. doi: 10.1542/peds.2009-3592
Serdar, M., Mordelt, A., Müser, K., Kempe, K., Felderhoff-Müser, U., Herz, J., et al. (2019). Detrimental impact of energy drink compounds on developing oligodendrocytes and neurons. Cells. 8, 1381. doi: 10.3390/cells8111381
Silva, C. G., Métin, C., Fazeli, W., Machado, N. J., Darmopil, S., Launay, P. S., et al. (2013). Adenosine receptor antagonists including caffeine alter fetal brain development in mice. Sci. Transl. Med. 5, 197ra.104. doi: 10.1126/scitranslmed.3006258
Vargiu, R., Broccia, F., Lobina, C., Lecca, D., Capra, A., Bassareo, P. P., et al. (2021). Chronic Red Bull consumption during adolescence: effect on mesocortical and mesolimbic dopamine transmission and cardiovascular system in adult rats. Pharmaceuticals 24;14, 609.550 doi: 10.3390/ph14070609
Wolk, B. J., Ganetsky, M., and Babu, K. M. (2012). Toxicity of energy drinks. Curr. Opin. Pediatr. 24, 243–51. doi: 10.1097/MOP.0b013e3283506827
Wu, G. F., Ren, S., Tang, R. Y., Xu, C., Zhou, J. Q., Lin, S. M., et al. (2017). Antidepressant effect of taurine in chronic unpredictable mild stress-induced depressive rats. Sci. Rep. 7, 4989. doi: 10.1038/s41598-017-05051-3
Zhang, H., Lee, Z. X., and Qiu, A. (2020). Caffeine intake and cognitive functions in children. Psychopharmacology 237, 3109–3116. doi: 10.1007/s00213-020-05596-8
Keywords: energy drinks, alcohol, caffeine, taurine, brain development, AMED, adolescence
Citation: Acquas E, Dazzi L, Correa M, Salamone JD and Bassareo V (2023) Editorial: Alcohol and energy drinks: is this a really good mix? Front. Behav. Neurosci. 17:1213723. doi: 10.3389/fnbeh.2023.1213723
Received: 28 April 2023; Accepted: 16 May 2023;
Published: 31 May 2023.
Edited and reviewed by: Liana Fattore, CNR Neuroscience Institute (IN), Italy
Copyright © 2023 Acquas, Dazzi, Correa, Salamone and Bassareo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Valentina Bassareo, bassareo@unica.it