Resumen
En las últimas décadas, el consumo de bebidas energéticas ha aumentado drásticamente, especialmente entre jóvenes, adolescentes y deportistas, impulsado por la búsqueda constante de efectos ergogénicos, como el aumento del rendimiento físico y cognitivo. Paralelamente, el consumo mixto de bebidas energéticas y etanol, bajo la modalidad de Binge Drink, ha crecido de manera similar entre los adolescentes. Sin embargo, poco se sabe si el consumo combinado de estas bebidas, durante la adolescencia, puede tener efectos a largo plazo sobre la función central, lo que plantea la cuestión de los riesgos de este hábito sobre la maduración cerebral. Biggio,etc.al.,(https://doi.org/10.1016/j.neuropharm.2024.109993) diseñaron este estudio para evaluar, mediante enfoques conductuales, electrofisiológicos y moleculares, los efectos a largo plazo sobre la plasticidad del hipocampo del etanol (EtOH), las bebidas energéticas (ED) o el alcohol mezclado con bebidas energéticas (AMED) en un modelo de binge-drink en ratas. . Los resultados muestran que la administración compulsiva de AMED produce cambios adaptativos en el hipocampo a nivel molecular, asociados a alteraciones electrofisiológicas y de comportamiento, que se desarrollan durante la adolescencia y aún son detectables en animales adultos. En general, el estudio indica que la exposición de los adolescentes a AMED al consumo excesivo de alcohol representa un hábito que puede afectar permanentemente la plasticidad del hipocampo.
En Detalle
Los datos epidemiológicos indican un aumento en el consumo de alcohol (EtOH) entre los adolescentes, que va desde un consumo bajo a intenso y un abuso patológico (Gutiérrez y Sher, 2015; Lees et al., 2020). Además, los consumidores jóvenes concentran su consumo de bebidas alcohólicas en un marco temporal muy restringido con un fenómeno conocido como binge drinking (Chung et al., 2018). Por lo tanto, el consumo excesivo de alcohol en adolescentes consumidores de EtOH representa un importante factor de riesgo para la salud (Hill et al., 2000; Mokdad et al., 2016), que necesita estrategias de prevención eficaces (Hawkins et al., 1992; Toumbourou et al., 2019) .
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Además, el consumo de EtOH a menudo se asocia con la ingesta de bebidas energéticas (DE) similares a los refrescos pero caracterizadas por altas concentraciones de estimulantes como la cafeína con ingredientes adicionales (taurina y vitaminas). Los DE se han vuelto muy populares debido a los efectos publicitados que tienen un atractivo particular para los usuarios jóvenes. De hecho, además del sabor agradable, los fabricantes afirman que estas bebidas pueden tener varias acciones «positivas», que incluyen aumento de la energía física, la concentración, el rendimiento deportivo, el metabolismo, la actividad mental y el estado de alerta (Vercammen et al., 2019; Verster et al. , 2012, 2015). Los adultos jóvenes, pero especialmente muchos estudiantes adolescentes, beben cantidades significativas de ED, con la expectativa de que mejoren su concentración y rendimiento cognitivo (Smit y Rogers, 2000; Specterman et al., 2005), les ayuden a mantenerse despiertos y reduzcan el cansancio físico , supuestamente impulsados a beber ED con la expectativa de contrarrestar los efectos del estrés diario relacionado con los compromisos de estudio (Mahoney et al., 2019). A partir de los análisis de datos informados en varios estudios, no está claro si el consumo de DE asociados con EtOH es beneficioso o perjudicial para la función cerebral (Alsunni, 2015; Arria et al., 2011; Brunborg et al., 2022; Cadoni y Peana, 2023; De Giorgi et al., 2022); De hecho, importantes factores de riesgo para el consumo de EtOH durante la adolescencia podrían estar representados por su asociación con una bebida energética (ED), es decir, alcohol mezclado con ED (AMED) (Acquas et al., 2023; Sefen et al., 2022). Es plausible pensar que algunas de las sustancias contenidas en los DE, como la cafeína y la taurina, que pueden influir por sí solas en el sistema de recompensa del cerebro (Vargiu et al., 2021), también pueden contribuir a la alteración de la sensibilidad al EtOH al influir en el sistema de recompensa cerebral y aumentar el riesgo de consumo nocivo de alcohol (Dazzi et al., 2024; Hsu et al., 2009; Lubman et al., 2007; Yasuma et al., 2021). Varias pruebas experimentales sugieren que la combinación de EtOH y cafeína durante la adolescencia puede aumentar el potencial de abuso de EtOH (Arria et al., 2011; O’Brien et al., 2008; Peacock et al., 2012; Thombs et al., 2011 ), pero se sabe muy poco sobre el impacto del consumo de AMED.
La adolescencia es un período de desarrollo caracterizado por la maduración cognitiva, emocional y neurobiológica (Dahl, 2004), y el factor neurotrófico derivado del cerebro (BDNF, por sus siglas en inglés) de neurotrofina desempeña un papel crucial en estos procesos (Cohen-Cory et al., 2010). La adolescencia también se caracteriza por la toma de decisiones altamente riesgosas y una mayor vulnerabilidad al abuso de alcohol (Crews et al., 2007). El impacto del consumo excesivo de alcohol entre los adolescentes se ha estudiado ampliamente en modelos con roedores. Varios estudios demostraron que dichas exposiciones tempranas al EtOH causan deterioro de la función cognitiva y la flexibilidad, aumento de la ansiedad social, desinhibición conductual e impulsividad (Beaudet et al., 2016; Coleman et al., 2011, 2014), que persisten hasta la edad adulta. Además, la exposición repetida al EtOH durante la adolescencia también aumenta la motivación para su consumo (Spear, 2018) y parece que los cambios en el BDNF son evidentes después de que el adolescente consume alcohol de forma habitual (Cutuli y Sampedro-Piquero, 2022). A medida que el cerebro adolescente experimenta una maduración neurológica significativa, el consumo de EtOH durante este período crítico tiene el potencial de interferir con el desarrollo normal y producir cambios neurológicos persistentes y déficits funcionales (Spear, 2000, 2018). Si bien hay evidencia clínica disponible sobre las consecuencias conductuales y funcionales de AMED (Roemer y Stockwell, 2017), y a pesar de la necesidad imperiosa de comprender mejor los costos en salud y diseñar estrategias preventivas para reducir los resultados negativos de este hábito adolescente, la mayoría de los estudios preclínicos se centró en el uso de altas dosis de EtOH y cafeína (Fritz et al., 2014) como modelo para caracterizar el impacto del consumo excesivo de alcohol de AMED en adolescentes en la edad adulta, sin tener en cuenta el consumo combinado de un DE completo (con todos sus ingredientes farmacológicamente activos) con una bebida a base de EtOH, especialmente en la adolescencia.
Para proporcionar un trasfondo traslacional aún faltante para una mejor comprensión de las consecuencias del consumo excesivo de alcohol en los TCA (es decir, AMED), con especial atención a la transición de la adolescencia a la edad adulta, en este estudio utilizamos un enfoque multidisciplinario para investigar si en la adolescencia temprana la administración de EtOH, ED o AMED en forma compulsiva tiene un impacto en la función cerebral de ratas jóvenes y adultas. En este sentido, un estudio anterior informó que el consumo combinado de ED, EtOH o AMED bajo la administración en forma compulsiva tiene efectos perjudiciales duraderos en la corteza prefrontal (Dazzi et al., 2024).
Para imitar una situación cercana a la real en adolescentes humanos que consumen cantidades moderadas de EtOH (Eckardt et al., 1998), los investigadores optaron por administrar, como lo hicieron en su estudio anterior (Dazzi et al., 2024), a cada animal, en cada sesión de tratamiento, con una cantidad de EtOH que corresponde a 1,5-2 tragos que contienen aproximadamente 12 g de EtOH (Eckardt et al., 1998; Kalant, 1975), para determinar más a fondo si dicho protocolo de consumo excesivo de alcohol de los adolescentes AMED la administración podría afectar el cerebro ya sea en la edad adulta y en la adolescencia, un período crítico del desarrollo donde los factores de crecimiento neuronal son cruciales para la maduración neurobiológica y desempeñan papeles importantes durante el desarrollo del cerebro participando en la formación de conexiones sinápticas apropiadas en el cerebro (Cohen-Cory et al., 2010). Por lo tanto, estudiaron los efectos conductuales inducidos por EtOH, ED o AMED sobre la locomoción, el aprendizaje y la memoria, así como los cambios electrofisiológicos y moleculares involucrados en la plasticidad sináptica, como la expresión de BDNF y su receptor de tirosina-quinasa trkB en el hipocampo de ratas adolescentes, y en diferentes cohortes, de ratas adultas. Además, también se midieron los niveles plasmáticos de corticosterona para evaluar una posible desregulación a largo plazo del eje hipotalámico-pituitario-suprarrenal inducida por la exposición de adolescentes al consumo excesivo de alcohol a EtOH, ED y AMED.
En resumen, partiendo del supuesto de que el consumo compulsivo de EtOH y DE durante la adolescencia pueden provocar alteraciones cognitivas y conductuales y cambios en la plasticidad del hipocampo que persisten en la edad adulta, era crucial evaluar en profundidad el efecto del consumo excesivo de alcohol en la adolescencia administración de bebida compulsiva de EtOH, ED o AMED en ratas jóvenes y adultas. Nuestros resultados muestran que el consumo de AMED durante el periodo periadolescente produce cambios adaptativos en el hipocampo a nivel electrofisiológico y molecular, asociados a alteraciones del comportamiento, que ya son detectables durante la adolescencia y persisten en la edad adulta. Esta conclusión se ve reforzada por el deterioro duradero de la función cortical prefrontal revelado por el protocolo idéntico de administración compulsiva de AMED de un estudio anterior (Dazzi et al., 2024). En general, el análisis de todo el conjunto de datos obtenidos sugiere fuertemente que la AMED, durante la adolescencia, puede tener resultados que no son necesariamente la suma de los observados con EtOH o ED solos y afectan permanentemente la plasticidad del hipocampo. Sin embargo, debe tenerse en cuenta que la interpretación de estos resultados puede ser limitada teniendo en cuenta las diferencias de sexo. Aunque el análisis de las supuestas diferencias sexuales merece atención, estaba más allá del alcance de este estudio y habría introducido la variable adicional de las fluctuaciones hormonales durante el ciclo estral. Es bien sabido que las hormonas gonadales y sus metabolitos neuroactivos modulan varios sistemas de neurotransmisión implicados en la respuesta al EtOH y contribuyen a las diferencias sexuales en los efectos del alcohol en el sistema nervioso central (Finn, 2023). Por lo tanto, sus fluctuaciones durante el ciclo estral podrían contribuir a una mayor variabilidad y la necesidad de utilizar un mayor número de animales para la experimentación con el fin de tener una evaluación precisa que pueda ser considerada en futuros estudios.
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