Proceedings of the 13th Alcohol Hangover Research Group Meeting in Dresden, Germany ^†

Abstract

These proceedings summarize the presentations of the 13th Alcohol Hangover Research Group meeting held 20–22 April 2023 in Dresden, Germany. The purpose of this annual meeting is to discuss current research on the causes, consequences and treatment of alcohol hangover, to network, and to establish future research collaborations. Various topics of interest were presented and discussed, including the impact of anxiety and personality on susceptibility for experiencing hangovers, sleep, the impact of the COVID-19 pandemic, the role of inflammation and alcohol metabolism in the pathology of alcohol hangover, novel treatments, and the changing regulatory landscape for hangover solutions.

1. Introduction

The 13th Alcohol Hangover Research Group (AHRG) meeting was held in Dresden, Germany, 20–22 April 2023, and organized by Joris Verster (Utrecht University, The Netherlands) and Ann-Kathrin Stock (TU Dresden, Germany). Joris Verster (Utrecht University, The Netherlands) presented an overview of the accomplishments of 13 years of collaboration of the members of the AHRG. Thirteen meetings were held across 4 continents where academic researchers and representatives of industry presented their latest research, discussed new research plans, and established collaborations [1,2,3,4,5,6,7,8]. The most notable achievements of the AHRG were consensus papers on hangover research methodology [9,10], and the development of a definition for the hangover [11,12]: The alcohol hangover refers to the combination of negative mental and physical symptoms which can be experienced after a single episode of alcohol consumption, starting when blood alcohol concentration (BAC) approaches zero [12]. The next sections provide an overview of the presentations held on current research on the causes, consequences and treatment of the alcohol hangover.

2. Personality, Mood, and Health Correlates

Anne Boogaard (Utrecht University, The Netherlands) summarized the literature on hangovers and personality. It is known that personality traits such as a higher level of extraversion and a lower level of conscientiousness have been related to increased alcohol consumption [13]. In this context, it has also been investigated to what extent personality influences the presence and severity of alcohol hangovers. For example, research by Harburg et al. [14,15] suggested that drinkers with higher neuroticism scores reported more severe hangovers. However, this study has several methodological limitations, questioning the reliability of this observation [16]. In a more recent study, Verster et al. [17] found that neuroticism and baseline mood were not significant predictors of hangover severity. Instead, subjective intoxication was the best predictor of hangover severity. Studies found that mental resilience levels, i.e., the psychological ability to bounce back, did not significantly differ between hangover-sensitive and hangover-resistant drinkers [18], and that the partial correlation between mental resilience and hangover severity was not significant when correcting for estimated BAC [19]. However, opposite findings were reported by Terpstra et al. [20] who found a negative correlation between mental resilience and hangover severity on the past month’s latest hangover occasion, i.e., higher levels of mental resilience were associated with experiencing less severe hangovers. In this study among Australian adults, baseline mood assessments of anxiety, stress, and depression also correlated significantly and positively with hangover severity on the past month’s latest hangover occasion. Some methodological issues may however have influenced these findings. That is, the partial correlation between mental resilience and hangover severity was computed using the hangover severity rating for participants’ latest hangover occasion. However, for the correction for the number of alcoholic drinks consumed, data from the past month’s heaviest drinking occasion was used. The latter may have significantly influenced the outcome of the correlational analyses, as the latest hangover occasion is not necessarily the same drinking occasion as the past month’s heaviest drinking occasion. A final study in 153 Dutch adults was discussed [16]. This study did control for alcohol consumption from the same drinking occasion as the hangover severity rating (i.e., both for the past month’s heaviest drinking occasion). To control for alcohol consumption, estimated BAC was used in the partial correlations. Correlations of hangover severity with the personality traits psychoticism, extraversion, and neuroticism were further corrected for social desirability (scores on the socialization scale). No significant correlations were found with hangover frequency and hangover severity and mental resilience, baseline mood, and personality traits. Taken together, it is unlikely that mental resilience, baseline mood, or personality have a relevant impact on hangover frequency and hangover severity. However, future studies are planned to further evaluate this.

Andy Kim (Dalhousie University, Canada) presented data on the relationship between anxiety and the alcohol hangover. A significant proportion of individuals, approximately 80%, are sensitive to hangovers, with around 30% reporting symptoms of depression and 20% reporting symptoms of anxiety during the hungover state [21]. Moreover, individuals with higher levels of non-hangover depression and anxiety are also more vulnerable to experiencing higher depression and anxiety during a hangover [22]. These symptoms can persist for several days, posing risks similar to those associated with non-hangover depression and anxiety symptoms [23]. A recent study examined the role of non-hangover depression, anxiety, and stress for hangover susceptibility [24]. This study included a sample of 5111 university students from The Netherlands and the UK: 3205 hangover-sensitive and 1906 hangover-resistant drinkers. Hangover-sensitive drinkers exhibited significantly higher levels of baseline anxiety and stress, but not depression, when compared to hangover-resistant drinkers. However, the observed group differences were small, with magnitudes of less than 1 out of 42 points on the DASS-21 subscales, and therefore unlikely to be clinically significant.

Research suggests that individuals with higher levels of depressive symptoms tend to engage in heavier drinking over time, which supports the self-medication hypothesis [25]. Conversely, individuals with higher levels of anxiety tend to consume alcohol less heavily over time [26]. This may be because anxious individuals learn to use alcohol in lower doses to avoid severe hangover anxiety but still capitalize on alcohol’s tension-relieving and social facilitation properties [27]. However, it should be noted that consuming alcohol can alleviate hangover symptoms, potentially contributing to the maintenance of drinking behavior [28]. Moreover, individuals who rely on alcohol to cope with depression and anxiety often experience problems associated with alcohol use, such as blackouts [29]. Thus, it is unclear if hangover depression and anxiety act as protective factors against future heavy drinking due to their aversiveness or if they confer vulnerability to future heavy drinking and alcohol problems if individuals increase alcohol consumption in response to hangover depression and anxiety as a coping mechanism. Future studies will continue to investigate these phenomena.

Benthe van der Weij (Utrecht University, The Netherlands) discussed how sleep after an evening of alcohol consumption can impact next-day hangover severity. Rohsenow et al. [30] conducted an experimental study evaluating sleep and the next-day ship power plant operation in maritime academy cadets. After a baseline day, half of the participants consumed alcohol to reach a BAC of 0.115%, while the other half were the alcohol-free control group on the second test day. The alcohol group showed significantly poorer performance on the ship power plant tasks. Surprisingly, both the alcohol group and the control group reported improved sleep on the second night of the experiment. The latter was likely due to the ‘first night effect’, i.e., participants had to get used to the new sleep environment. In a subsequent study [31], hangover, sleep, and next-day neurocognitive performance were assessed in 95 young adults. In this study, sleep was assessed by both self-report and polysomnography. On the hangover day, participants reported poorer sleep quality and increased daytime sleepiness. Polysomnography results revealed they spent a shorter time in REM sleep, had more slow wave sleep, and increased wake time after alcohol consumption. No significant changes were found for total sleep time, percent of the time in Stage 1 or 2 sleep (i.e., light sleep), or sleep onset latency. Poorer sleep and increased daytime sleepiness were associated with having more severe hangovers. In a third study, Rohsenow et al. [32] compared sleep and hangover severity after consuming beer with or without caffeine (383 mg of caffeine, the equivalent of about 4 cups of coffee) in a population of young adults. Compared to the non-caffeine group (n = 36), adding caffeine to alcohol (n = 28) had no significant effect on total sleep time or sleep latency, hangover severity, or sleepiness the morning after drinking to intoxication (peak BAC 0.12%). In addition to these experimental studies, several surveys examined the relationship between sleep and the hangover. A first survey among 335 Dutch adults confirmed that sleep quality was significantly worse after an evening of alcohol consumption [33]. However, although hangover severity correlated significantly and positively with daytime sleepiness, the correlation between sleep quality and hangover severity was not significant. A second survey was conducted among 785 Dutch students [34]. The participants reported on their latest heavy drinking occasion. Compared to a regular (alcohol-free) night, total sleep time was significantly shorter after the drinking occasion. Total sleep time was negatively correlated with hangover severity and hangover duration. Thus, a shorter total sleep time was associated with experiencing more severe hangovers of longer duration. However, these findings were not replicated in a naturalistic study among 25 students, that assessed sleep objectively with an actigraphy watch after an evening of alcohol consumption and an alcohol-free night [35]. Surprisingly, hangover severity did not correlate significantly with any of the sleep outcomes. Finally, Ayre et al. [36] conducted a semi-naturalistic study that confirmed previous findings: shorter total sleep time, poorer sleep quality, a greater number of nightly awakenings, and a longer duration of these nightly awakenings were all significantly associated with greater hangover severity. Taken together, although sometimes inconsistent findings have been reported, it can be concluded that shorter total sleep time and poorer sleep quality are associated with experiencing more severe hangovers.

3. Neurocognitive Functioning

Darren Kruisselbrink (Acadia University, Canada) discussed cognitive efficiency in neurocognitive and physical tasks across hangover and control conditions. Impairments of neurocognitive and physical performance during the alcohol hangover have not been consistently shown in hangover research. Effort is a critical factor in task achievement but its role in relation to performance during a hangover has received little attention. Paas and van Merrienboer [37] developed a computational method that combines measures of effort and performance to establish a relative measure of efficiency across various experimental conditions. They considered one experimental condition (e.g., hangover) to be less efficient than another (e.g., control) if participants reported giving more effort to produce similar levels of performance or if, when they gave similar levels of effort, they performed worse. The aim of the presented study was to examine the efficiency of effort under three conditions: (1) control, (2) after an evening of light drinking—light hangover, and (3) after a night of heavy drinking—heavy hangover.

Participants (n = 17) indicated their typical alcohol consumption on light and heavy drinking nights and were asked to follow these consumption patterns on the light and heavy drinking nights of their choosing. On drinking nights they consumed commercially packaged drinks, texting photos of each drink to a research assistant in real time. Upon arriving at the lab ~12 h after finishing their last drink, a BAC of zero was confirmed with a breathalyzer test. Participants then completed (1) a composite 23 item hangover symptom severity scale (anchors 0–10), (2) a test battery consisting of a physical task (grip strength), a coordination task (Minnesota Manual Dexterity One Hand Turning and Placing test), and two neurocognitive tasks testing working memory and processing speed (Trail Making B test; Symbol-Digit Modalities Test), and (3) a category-ratio scale measure of effort following each task.

Participants consumed a mean (SD) 63.2 (27.8) g alcohol over approximately 2 h on their light drinking night and 122.5 (38.4) g over approximately 4 h on their heavy drinking night. Hangover severity was rated as 31.8 (28.4) and 70.0 (37.4) the afternoon following light and heavy drinking, respectively. Across the experimental tasks, the pattern of results showed that efficiency was highest in the control condition, and lowest in the heavy hangover condition. In the light hangover condition, both high and low efficiency scores were found. In conclusion, integrating the performance–effort relationship into a computed efficiency score can provide a more nuanced insight into the relationship between performance, effort, and hangover and shows promise for more reliably demonstrating impairments during hangover.

4. Hangover Symptoms and Their Severity

The presence and severity of hangover symptoms differs between individuals, but also varies from drinking occasion to drinking occasion. In addition, while most people who drink alcohol are familiar with experiencing hangovers (i.e., hangover-sensitive drinkers), a significant subgroup of about 10–20% of drinkers report experiencing no hangovers, despite consuming the same amounts of alcohol (i.e., hangover-resistant drinkers) [10].

Joris Verster (Utrecht University, The Netherlands) discussed research comparing the next-day symptoms after an evening of alcohol consumption of hangover-sensitive and hangover-resistant drinkers. A semi-naturalistic study was conducted including an evening of alcohol consumption and an alcohol-free control day [38]. Throughout the day following the drinking occasion or control day (09:30 until 15:30), the presence and severity of 23 hangover symptoms, as well as mood (Profiles of Mood States-Short Form), and daytime sleepiness (Karolinska Sleepiness Scale) were assessed. On the alcohol day, there was no significant difference in alcohol consumption or total sleep time between the hangover-sensitive drinkers and the hangover-resistant drinkers. The most frequently reported and most severe symptoms reported by the 15 hangover-sensitive drinkers were sleepiness, fatigue, concentration problems, and headache. The hangover symptoms severity gradually decreased during the day, but most reported that symptoms were still present in the afternoon. Compared to the control day, the 14 hangover-resistant drinkers reported either no symptoms, or only the presence of mild fatigue and reduced vigor. These mild sleepiness-related symptoms were most likely due to sleep loss, as the drinking occasion shortened total sleep time on the alcohol day.

Ann-Kathrin Stock (TU Dresden, Germany) addressed the question of whether the severity of alcohol hangover can be predicted from alcohol sensitivity ratings as assessed with the Alcohol Sensitivity Questionnaire (ASQ) [39,40]. To this end, the preliminary analysis of the data of n = 92 healthy young males who had completed the ASQ before undergoing an experimentally induced binge-like breath alcohol concentration of ~0.12% and subsequent hangover was presented and discussed. The data suggested that the subjective rating of the severity of alcohol hangover after an experimentally standardized, binge-like alcohol intoxication was not correlated with age, height, weight, breath alcohol levels reached during drinking, or with the previously assessed ASQ light score, ASQ heavy score, or the hangover-specific item from the ASQ. Taken together, these findings suggest that retrospective information about alcohol sensitivity as assessed with the ASQ is not well-suited to predict the severity of real-life alcohol hangover. Possible reasons for these findings as well as other, more promising potential predictors (including sleep quality, inflammation, histamine release, and dehydration) were discussed.

5. Pathology

Marlou Mackus (Utrecht University, The Netherlands) discussed the current evidence on the pathology of the alcohol hangover. Research on the pathology of the alcohol hangover revealed that it is not caused by dehydration [41], but that differences in ethanol metabolism [42] and, in particular, the inflammatory response to alcohol consumption [43,44] determine the presence and severity of hangover symptoms. The content of this presentation focused on alcohol metabolism. Research demonstrated that individuals who break down ethanol more quickly report less severe hangovers [42,45]. A significant positive correlation between urine ethanol concentration and hangover severity was previously reported [46], and another study demonstrated that the ethanol breakdown rate, as assessed via breathalyzer, was significantly associated with hangover severity [45]. Together, these findings suggest that a quick breakdown of systemic ethanol results in less ethanol entering the brain, and subsequently in less severe hangovers.

Agnese Merlo (Utrecht University, The Netherlands) presented a study that further investigated the inflammatory response to alcohol consumption and immune fitness [47]. The naturalistic study in 15 hangover-sensitive drinkers and 14 hangover-resistant drinkers comprised an alcohol test day and an alcohol-free control day. For both occasions, the next-day assessment of biomarkers of immune functioning were conducted hourly (09:30 until 15:30). The assessments were made in saliva and included interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α. In addition, immune fitness (i.e., the capacity of the body to respond to health challenges (such as infections) by activating an appropriate immune response) [48] was assessed. Overall hangover severity was assessed with a single-item rating scale, ranging from 0 (absent) to 10 (severe) [49]. No significant group differences were found in the amount of alcohol consumed on the alcohol day (around 13 alcoholic drinks (130 g)). Whereas the hangover-resistant group reported no hangover, the hangover-sensitive drinkers reported a hangover severity score of 6.1 in the morning, which decreased during the day to 3.3 in the afternoon. For the hangover-sensitive group, the IL-6 concentration at 09:30 on the alcohol day was significantly higher compared to the control day. This effect was not seen for the hangover-resistant group. No significant differences between the groups were found at other timepoints. No significant differences between the alcohol day and control day were found for the other biomarkers.

The immune fitness of the hangover-sensitive group on the control day was significantly poorer compared to the hangover-resistant group. This observation is in line with previous survey findings [50]. For both groups, a significant reduction in immune fitness was reported on the alcohol day. However, the magnitude of the effect of alcohol consumption on next-day immune fitness differed significantly between the groups. That is, whereas the reduction in immune fitness of the hangover-resistant group was modest and scores on both test days were around 7.5 (out of 10), indicating an adequate immune fitness, the immune fitness scores on the alcohol day of the hangover-sensitive group were below 6, indicating reduced immune fitness. Taken together, the alcohol hangover was associated with significantly increased saliva IL-6 concentrations and significantly reduced immune fitness. These findings confirm the importance of the inflammatory response to alcohol consumption in the development of the alcohol hangover.

Analia Karadayian (University of Buenos Aires, Argentina) discussed the mechanism underlying ethanol after-effects in brain bioenergetics. The brain is one of the tissues that are most negatively affected by ethanol after-effects. In fact, many of the motor impairments and unpleasant symptoms that occur during alcohol hangover are primarily due to alterations in neural pathways. The detrimental effects of alcohol consumption on the central nervous system stem from the disruption of macromolecules caused by an increase in the generation of oxidizing species. This leads to processes such as lipid peroxidation, protein carbonylation, and damage to deoxyribonucleic acid [51].

Animal models demonstrated that the hangover is associated with long-lasting effects on motor and affective behavior for at least 14–20 h [52,53]. According to this evidence, the after-effects of acute ethanol exposure were linked to an imbalance in the production of free radicals and antioxidants. This imbalance was accompanied by reductions in oxygen consumption, inhibition of enzymatic activity in the respiratory chain complex, and declines in mitochondrial membrane potential observed in the mouse brain cortex and cerebellum [54,55,56]. Recent data indicates that most biochemical alterations due to hangover occur specifically in the mitochondria present at brain cortex synapses. Particularly, the mitochondria at the synapses exhibited exacerbated levels of reactive oxygen species, damage to lipids, decreases in enzymatic and non-enzymatic antioxidants, and mitochondrial dysfunction [57,58]. Moreover, ethanol could exert its negative after-effects on the nitric oxide metabolism by reducing the expression of the protein complex N-methyl-D-aspartate receptor, postsynaptic density protein-95, and neuronal nitric oxide synthase proteins, decreasing the activity of neuronal nitric oxide synthase, and affecting calcium entry at the synapses [59]. It is widely known that mitochondrial dysfunction and oxidative stress could lead to cell death by the activation of mitochondrial apoptotic signaling pathways.

Alcohol hangover results in the loss of mitochondrial granularity and triggers a significant increase in mitochondrial permeability, potentially leading to mitochondrial swelling. This is also accompanied by the induction of Bax and cytochrome c translocation from the mitochondria to cytosol, which clearly indicates the intrinsic apoptotic pathway activation. The protein expression of caspase 3, 8, and 9 was enhanced together with the increase in the activity of caspase 3 and 6 due to the hangover condition [60]. Beyond the activation of the mitochondrial apoptotic pathway, alcohol after-effects could result in the activation of the Poly ADP-ribose polymerase 1 (PARP1)-mediated cell death program which involves the increment in both p53 and PARP1 protein expression and a strong reduction in sirtuin 1 (SIRT-1) that, at basal conditions, promotes mitochondrial biogenesis and DNA repair [61]. In conclusion, alcohol after-effects could result in the activation of two interrelated mechanisms in the brain cortex: the induction of mitochondrial apoptotic signaling pathways, and the PARP1-mediated cell death program [60].

The possible role of ethanol metabolites for apoptotic triggering should be taken into consideration. Acetaldehyde has been postulated to induce apoptosis via oxidative stress and Ca²⁺ imbalance [62]. As such, acetaldehyde could be primarily responsible for the detrimental effects of binge ethanol exposure on mitochondrial bioenergetics in brain synapses. Understanding these mechanisms can provide valuable insights for the development of targeted interventions to alleviate the negative consequences of alcohol hangovers. Further research is warranted to explore potential therapeutic strategies aimed at mitigating acetaldehyde-mediated effects and promoting recovery from alcohol-induced mitochondrial impairment.

6. Current and Future Hangover Treatments

Joris Verster (Utrecht University, The Netherlands) discussed the dynamic market of hangover products currently sold in the USA. In December 2019, the hangover products available on the website Amazon.com were evaluated [63]. The search revealed 82 products, which were all supplements. The most frequently found ingredients were vitamin B1 (58.5% of the products), vitamin B6 (54.9% of the products), milk thistle extract (48.8% of the products), dihydromyricetin/ DHM (47.6% of the products), and N-acetyl L-cysteine/ NAC (45.1% of the products). Of the 82 products, 53 (64.6%) made disease claims which are not allowed for supplements.

A follow-up study was conducted in April 2023 [64]. Significant changes were seen in the hangover product landscape. During the COVID-19 pandemic, the number of available hangover products was reduced to 38, i.e., a reduction of 53.7%. Although the US Food and Drug Administration (FDA) sent several warning letters to companies that made disease claims [65,66], half of the companies (50%) in the new search still made such claims for their product. Other FDA warning letters concerned the inclusion of NAC as an ingredient [67]. NAC is an FDA-approved medicine since 1963 and is therefore not allowed as an ingredient of supplements. The latter did have an impact on the hangover market, as in 2023, only one hangover product included NAC as an ingredient. In 2023, the most frequently reported ingredients of hangover products on the US market were DHM (52.6% of the products), vitamin B1 (42.1% of the products), vitamin B12 (42.1% of the products), sodium (42.1% of the products), and vitamin B6 (39.5% of the products). There is no scientific evidence from double-blind, placebo-controlled clinical trials in humans for any of the available products that show that the products are effective. DHM continued to be a popular ingredient, despite research showing that it is not effective in preventing or reducing alcohol hangover [68]. Taken together, the US hangover product market has significantly changed between 2019 and 2023. It is important to continue monitoring market developments, both in the USA and other parts of the world.

Jacqueline Iversen (Sen-Jam Pharmaceutical, Huntington, NY, USA) presented a new hangover treatment, SJP-001, which is currently in development by Sen-Jam Pharmaceutical. Since the alcohol hangover is treated as a disease by the US FDA, the company aims to obtain FDA approval to market SJP-001 as a medicine. SJP-001 is a combination product of two existing over-the-counter (OTC) oral drugs, the non-steroid anti-inflammatory drug naproxen and the antihistamine drug fexofenadine. Both naproxen [69] and fexofenadine [70] exhibit anti-inflammatory properties. The anti-inflammatory mechanism of action of SJP-001 is thought to prevent or reduce the alcohol hangover. A pilot study [71] revealed that compared to the placebo, SJP-001 significantly reduced hangover severity. Although promising, the sample size of the study was small and the findings should be verified in a large sample in a double-blind, placebo-controlled trial, including the assessment of biomarkers of immune functioning to further evaluate the mechanism of action of SJP-001.

Jakub Urbański (Nomi Biotech, Złotniki, Poland) presented the hangover product Alcorythm. The functional beverage Alcorythm aims to prevent or reduce hangovers by accelerating the breakdown of acetaldehyde, thereby reducing the inflammatory response to alcohol consumption. Alcorythm is intended to be consumed before alcohol consumption. The main ingredient of Alcorythm is NOMICU^® L-100, which contains a high concentration of curcuminoids (25–30%), which is much higher than other market-available formulations of curcumin. Additional ingredients include glucose and vitamin B complex. The results of a survey among 35 consumers were presented. The survey revealed that 67% of consumers reported feeling much better the day after alcohol consumption when using Alcorythm compared to the hangover they experience when not taking any treatment. Double-blind, placebo-controlled clinical trials are planned to further evaluate the efficacy and safety of Alcorythm.

7. Regulatory Developments

Emina Išerić (Utrecht University, The Netherlands) discussed the recent changes in the regulatory landscape for alcohol hangover solutions. Important new developments were discussed, including the fact that the World Health Organization (WHO) has adopted the definition of the alcohol hangover [72], defining the alcohol hangover as a combination of negative mental and physical symptoms which can be experienced after a single episode of alcohol consumption, starting when blood alcohol concentration (BAC) approaches zero [12]. In addition, the alcohol hangover gained a new status in the International Classification of Diseases, 11th edition (ICD-11). Until now, the alcohol hangover was wrongly listed as a synonym for intoxication. After discussion with the WHO, hangover is now listed as a separate entity [72]. The new classification of alcohol hangover in the ICD-11 as a separate entity may fuel the discussion about whether the alcohol hangover should be viewed as a disease. In the USA, disease claims are not allowed for hangover treatments, unless these are registered medicines [73,74]. According to the US FDA, disease claims are prohibited for dietary supplements. The current developments may have a significant impact on the future hangover product market, which currently mainly consists of dietary supplements.

8. COVID-19, Alcohol Consumption, and Hangovers

Agnese Merlo (Utrecht University, The Netherlands) presented data on alcohol consumption and hangovers during the COVID-19 pandemic. Research has investigated the overall changes in alcohol consumption patterns during the COVID-19 pandemic and associated lockdowns, as well as key correlates of increased alcohol use. Studies focusing on student populations in The Netherlands [75] and Argentina [76] provided insights into these trends. Overall, the COVID-19 pandemic has led to notable shifts in drinking behaviors. Approximately 25% of respondents in The Netherlands and Argentina reported an increase in alcohol consumption, while about 25% reported a decrease, and about 50% maintained their usual drinking habits. In line with the general literature [77], certain demographic and psychological factors were identified as significant correlates of increased drinking, including being female, and experiencing poorer mental health outcomes, such as higher levels of stress, anxiety, and depression. For some students, lockdown periods were also associated with increased weekly alcohol consumption and a higher number of drinking days. While the latter is an important group of drinkers to investigate further, around 75% of students reported a reduction or no change in alcohol consumption during the COVID-19 pandemic. In line with this, 47% of students in The Netherlands reported experiencing fewer hangovers during the COVID-19 lockdown periods, while 14% reported an increase in hangovers [75]. In Argentina, students exhibited significant reductions in weekly alcohol consumption during the lockdown periods, and a significantly lower hangover severity following their heaviest drinking occasion [76]. Post-pandemic research is necessary to monitor if changes in alcohol consumption and experiencing hangovers during the COVID-19 pandemic were temporary or persisted when life returned to normal.

9. Discussion

At the 13th AHRG meeting, several important new developments were discussed. The discussions on current and future hangover treatments highlight the urgent need for new, effective, and FDA-approved drugs that could prevent or mitigate the effects of alcohol hangover. The current alcohol hangover market consists solely of supplements which have not been tested in clinical trials or proven effective. In addition, some of these marketed supplements still contain products that have been proven to be ineffective for treating hangovers, such as DHM. It is evident that the current alcohol hangover market must change, particularly given the new classification of the hangover as a separate entity in the ICD-11 by the WHO. This adaptation reinforces the FDA regulations that dietary supplements should not make disease claims. In the interest of consumers, it is important that scientific research is conducted to evaluate the efficacy and safety of marketed hangover products, irrespective of whether these are FDA-approved drugs or supplements.

Understanding alcohol hangover pathology can aid in developing such treatments. Novel findings from studies involving both animal models and human subjects were presented during the meeting. These studies resolved the misconception that hangovers are primarily due to dehydration [41], instead indicating that the main contributing factors are ethanol metabolism and the body’s inflammatory response to alcohol intake [42,43]. Differences in the inflammatory response were investigated and confirmed between hangover-sensitive and hangover-resistant subjects. Hangover-sensitive individuals generally exhibit lower immune fitness and are more prone to higher inflammatory responses to alcohol consumption, as indicated by elevated IL-6 levels in saliva. These findings were put into practice, as demonstrated by the development of new hangover products currently underway such as SJP-001 and Alcorythm. However, both treatments need to undergo further testing in large, placebo-controlled clinical trials to confirm their effectiveness in preventing or reducing alcohol hangovers and demonstrate their corresponding mechanisms of action.

Several speakers provided an overview of studies evaluating the relationship between alcohol hangover and mood, personality and health correlates, such as sleep, mental resilience, anxiety and stress. Regarding the correlations with personality aspects such as neuroticism and mental resilience with hangover severity, inconsistent findings were reported. However, the studies that reported significant correlations between these correlates and the hangover also had methodological limitations. Other studies indicate that individuals with higher baseline anxiety and depression levels are more likely to experience severe hangover symptoms, though the relationship is complex and influenced by the presence or absence of adequate coping mechanisms. Additionally, research suggests that poor sleep quality and shorter sleep duration following alcohol consumption are generally associated with more severe hangovers.

Lastly, the impact of alcohol hangovers on cognitive and physical performance was discussed, highlighting that hangovers after heavy drinking lead to lower efficiency in tasks such as grip strength, memory, and coordination. Further research should explore how alcohol hangovers affect potentially dangerous daily activities such as operating heavy machinery or driving a car.