Introduction

Among young adults, there seems to be a habit of drinking energy drinks in tandem with alcohol (Tarragon et al., 2021). Perhaps it's part of a futile effort to sober up quickly (Ferré & O'Brien, 2011). Either way, countless research studies have identified dangerous behaviors associated with this practice, such as increased alcohol consumption (Marczinski 2015). Though, not nearly as many studies explored how energy drinks affect the brain after drinking alcohol. In a 2020 research study published in the aptly titled journal Alcohol, Hansen et al. examine the effects of one popular ingredient added to energy drinks, taurine, on brain recovery during alcohol withdrawal. Researchers administered taurine to rats undergoing withdrawal from chronic alcohol use. Hansen et al. hypothesized that taurine's potential neuroprotective qualities might help restore balance within neural receptors damaged by alcohol consumption (Hansen et al., 2020). Findings suggest that taurine's effects on receptors at different stages of alcohol consumption are complex. However, at the withdrawal stage, these effects aren't significant enough to support their hypothesis (Hansen et al., 2020). Research into ways to alleviate alcohol withdrawal can help treat chronic use and addiction––or, at least, may help ease your next hangover. 

Background

To understand what makes alcohol withdrawal such a ruthless experience, we must discuss what happens right before the withdrawal. Alcohol, more formally known as ethanol, acts in our brain in two main ways: by enhancing GABA (which inhibits neural activity) and blocking glutamate (which is usually excitatory) (Costardi et al., 2015). In chronic alcohol use, GABA and glutamate receptors (namely GABA_A and NMDA, respectively) adapt to counteract alcohol's inhibitory effects (Roberto & Varodayan, 2017). Alcohol can even change the genetic expression of these receptors (Osechkina et al., 2016). These adaptive mechanisms underly tolerance and dependence, which consequently create the hellish experience of alcohol withdrawal. Within our bodies, taurine is naturally produced and is key to restoring damaged tissue (Chen et al., 2019). In energy drinks, it's used as an antioxidant to improve athletic performance. In 2017, Hansen et al. observed behaviors in rats that suggested taurine might've alleviated alcohol withdrawal symptoms (Hansen et al., 2017). At the time, researchers couldn't explain such findings on a neurobiological level. Their 2020 study looked at taurine once more by inspecting its effects on GABA_A and NMDA receptors during withdrawal. 

Methods

Neural receptors are made of protein building blocks called "subunits." Subunit configurations make each receptor unique in its function (Zhu et al., 2016). Genetic expression of these subunit proteins can be observed by tracking the expression of associated mRNA. In this study, researchers put rats through a timeline of chronic alcohol consumption and consequent withdrawal. For 28 days (five consecutive business days each week), researchers gave distilled water to some rats and alcohol to others. From day 29 to day 33, all rats stopped receiving either alcohol or water, which induced a five-day-long withdrawal period. Across the five days, both "sober" and "alcohol" groups were given either taurine or placebo. Afterward, these rats were euthanized, and mRNA samples from their hippocampi were processed via qPCR to identify the expression of different subunits. Hippocampus––the memory and learning center of the brain––was chosen for this study because of its established role in maintaining the cycle of addiction (Koob & Volkow, 2010). Rates of each subunit's expression were compared to the rates of expression of other subunits, namely four GABA_A and two NMDA subunits. Because alcohol disrupts correlations between the expression of various subunits (Roberto & Varodayan, 2017), one may hypothesize that taurine would promote the restoration of these correlations during the withdrawal. 

Findings

In 2017, Hansen et al. performed an open-field-test on rats, which is used to examine behavioral trends of rats as they explore an open field. Control rats tended to be more curious and explorative in the open field than rats who were intoxicated or withdrawing. Taurine administration restored the exploratory behavior of withdrawing rats (Hansen et al., 2017). These findings suggested that taurine’s restorative effects alleviated withdrawal symptoms.

In 2020, the group repeated taurine administration to withdrawing rats. Researchers looked more closely at the expression of various receptor subunits within the hippocampus. They observed that with taurine administration only, without any alcohol, a positive correlation between two GABA_A receptor subunits (α1 and γ) emerged. The implication of this correlation is unclear; yet, it’s unlikely to be related to anything alcohol does since this correlation was observed in a group which wasn’t given any alcohol (control group). Some correlations between NMDA and GABA_A were lost to chronic alcohol use. Administration of taurine didn’t restore these correlations. Instead, taurine created novel correlations between NMDA and GABA_A which ultimately had no long-term implications. Most interestingly, the rats who were given taurine lost all correlations between all subunits, including those that existed before taurine administration and those induced by either alcohol or taurine during chronic use. Such a lack of reliable patterns in changes of correlations makes conclusions quite tricky to draw. Taurine’s effects seem to contradict one another depending on the stage of the experiment at which it was administered. Administration of taurine before or during intoxication created new correlations, but it was also deleterious to existing correlations during withdrawal. It’s unclear whether this removal of correlations has a positive, negative, or no effect on the rat brains’ functioning. Hansen et al.’s 2020 study provides no conclusive evidence to support the hypothesis that taurine’s restorative effects on NMDA and GABA_A receptors are what improved withdrawal symptoms in their 2017 experiment. 

Discussion

Per the Centers for Disease Control and Prevention, excessive alcohol use kills around 93,000 Americans each year (CDC, 2020). Chronic alcohol consumption can lead to Alcohol Use Disorder, which can cause severe alcohol withdrawal (American Psychiatric Association, 2013). Alcohol withdrawal symptoms can range from a mild migraine to a life-threatening medical emergency (Perciballi et al., 2018). On both ends of the severity spectrum, anything that may help relieve symptoms is a saving grace. Based on this article’s findings, it’s unlikely that taurine’s effects are clinically significant enough to be used in the treatment of severe withdrawal. In Hansen et al.’s 2020 study, taurine’s influence on subunit correlations didn’t have enough of a discernable pattern to have any utility. Though, their 2017 findings––which observed taurine’s ability to alleviate withdrawal symptoms in rats––still warrant future research into the neurobiological underpinnings of taurine’s impact on alcohol withdrawal. Perhaps taurine does affect withdrawal, but thus far, researchers proposed the wrong hypothesis to explain such effects and may need to investigate further. In the meantime, an energy drink might still help manage symptoms of the occasional mild hangover. High concentrations of caffeine within energy drinks might provide comfort for such hangovers (Ferré & O’Brien, 2011). Though, that comfort likely won’t be due to taurine’s effects on GABA_A or NMDA receptors. Regardless, the ultimate way to attenuate a hangover is to drink responsibly!

[+] References

[+] Other Work By Anastasiya Kozlovska