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Proceeding of the 9th Alcohol Hangover Research Group Meeting
Abstract
Background:
Alcohol hangover is a common occurrence among individuals who have experienced an episode of heavy alcohol consumption the previous night. Until now defined as the general feeling of misery that develops once the Blood Alcohol Concentration approaches zero. Despite its prevalence and several related adverse consequences, insufficient research has been conducted with regards to this matter and further understanding of the pathology of alcohol hangover is necessary. During the 9th Alcohol Hangover Research Group meeting, held on April 29th 2017, Utrecht, The Netherlands, numerous aspects of alcohol hangover were presented and many advances with regards to determinants, biological and cognitive consequences and potential treatment have been presented.
Conclusion:
Precisely, a definition of alcohol hangover has been established and wider understandings of biological and cognitive effects, alcohol metabolism, immune functioning and potential treatment of alcohol hangover were presented and discussed. Further research and development are necessary to attain a wider understanding of the pathology of alcohol hangover.
... The objectives of these meetings are to discuss recent findings and future research directions, to raise the profile of alcohol hangover research, and to start new research collaborations. Over the past 10 years, 11 successful AHRG meetings have been held across the world [5][6][7][8][9][10][11]. In 2010, the first AHRG meeting was held as a satellite symposium of the Research Society on Alcoholism conference in San Antonio, Texas, USA. ...
... (The Netherlands), and Wailoaloa Beach, Nadi in 2019 (Fiji). Proceedings of most of the AHRG meetings have been published [5][6][7][8][9][10][11]. ...
The alcohol hangover is defined as 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. Here, we present the book “The alcohol hangover: causes, consequences, and treatment”, written to celebrate the 10th anniversary of the Alcohol Hangover Research Group (AHRG), summarizing recent advances in the field of alcohol hangover research.
... Alcohol hangover is a phenomenon that occurs the day after the ingestion of alcohol, once the blood alcohol concentration (BAC) is approaching nil [1], and it is associated with a wide variety of symptoms, such as headache, nausea, and concentration problems [2,3]. Hangover is thought to be a considerable cause of economic loss through workplace absenteeism and lost productivity [4]. ...
... This may reinforce the need for an objective measure of hangover. However, research into biomarkers of hangover severity has yet to find a reliable indicator [1,28]. An alternative approach to measuring hangover severity in a more objective manner may be to examine the cognitive effects of hangover. ...
Alcohol hangover is a cause of considerable social and economic burden. Identification of predictors of alcohol hangover severity have the potential to contribute to reductions in costs associated with both absenteeism/presenteeism and health care. Pain catastrophising (PC) is the tendency to ruminate and describe a pain experience in more exaggerated terms. The current study examines the possibility that this cognitive coping strategy may influence experience of alcohol hangover. The aims of the current study were to (1) examine the relationship between hangover severity and PC, (2) explore and identify discreet factors within the Acute Hangover Scale (AHS) and (3) explore whether independent factors/dimensions of acute hangover are differentially predicted by PC. A retrospective survey (n = 86) was conducted in which participants completed the Acute Hangover Scale (AHS); the Pain Catastrophising Scale (PCS); a questionnaire pertaining to the amount of alcohol consumed; and a demographic information questionnaire. Regression analyses showed a significant relationship between PC and hangover severity scores and demonstrated that PC was, in fact, a stronger predictor of perceived hangover severity than estimated peak blood alcohol concentrations (eBACs). Factor analysis of the AHS scale, resulted in the identification of two distinct symptom dimensions; ‘Headache and thirst’, and ‘Gastric and cardiovascular’ symptoms. Regression analyses showed that both eBAC and PCS score were significantly associated with ‘Headache and thirst’. However, only PCS score was associated with ‘Gastric and cardiovascular’ symptoms. These novel findings implicate a role for cognitive coping strategies in self-reports of alcohol hangover severity, and may have implications for understanding behavioural response to hangover, as well as suggesting that hangover and PC may be important factors mediating the motivation to drink and/or abuse alcohol, with potential implications in addiction research. Furthermore, these findings suggest that distinct alcohol hangover symptoms may be associated with different mechanisms underlying the experience of alcohol hangover.
... Alcohol-induced headache (hangover headache) is among the most common types of headache, but the mechanism through which alcoholic drinks cause headaches remains unclear (1,2). Most clinical studies of hangovers have been retrospective, and the pathophysiological mechanisms that lead to headaches caused by alcoholic drinks have not been well-studied. ...
Objectives:
The present study aims to establish and evaluate a rat model for hangover headaches caused by alcoholic drinks.
Materials and methods:
Chronic migraine (CM) model rats were divided into 3 groups, and intragastrically administered alcoholic drinks (sample A, B, or C) to simulate hangover headache attacks. The withdrawal threshold for the hind paw/face and the thermal latency of hind paw withdrawal were detected after 24 hr. Serum was collected from the periorbital venous plexus of rats in each group, and enzymatic immunoassays were used to determine the serum levels of calcitonin gene-related peptide (CGRP), substance P (SP), and nitric oxide (NO).
Results:
Compared with the control group, the mechanical hind paw pain threshold was significantly lower in rats administered Samples A and B after 24 hr; however, no significant difference was observed across groups for the thermal pain threshold. The mechanical threshold for periorbital pain was only significantly reduced in rats administered Sample A. Immunoassays further indicated that serum levels of SP in the group administered Sample A were significantly higher than those in the control group; the serum levels of NO and CGRP were significantly higher in the group of rats receiving Sample B.
Conclusion:
We successfully developed an effective and safe rat model for investigating alcohol drink induced hangover headaches. This model could be used to investigate the mechanisms associated with hangover headaches for the development of novel and promising candidates for the future treatment or prophylaxis of hangover headaches.
The hangover is the most commonly reported negative consequence of alcohol use with several studies reporting the detrimental consequences of hangover on health, economy, and society. Research has emphasized the socioeconomic consequences of experiencing these physical and psychological symptoms in relation to absenteeism, increased risk of having accidents and injuries, and impairment of daily activities, such as job performance and driving a car. During the 10th Alcohol Hangover Research Group meeting, held on 29 April 2018, in Utrecht, The Netherlands, aspects of alcohol hangover were presented with regards to determinants, biological and cognitive consequences and potential treatments. Precursory and posterior factors influencing alcohol hangover, including biological, psychological, behavioral, metabolic aspects, cognitive functioning, and the role of the immune system in the development of alcohol hangover, were presented. In addition, potential preventive measures and treatments of alcohol hangover to reduce the adverse consequences of alcohol consumption and hangover symptoms were discussed. One study revealed that an average of 24% of social and heavy drinkers claimed not to experience hangover symptoms across time. Another study showed that food intake (either healthy or junk food) had no significant impact on next-day hangover severity. Research examining cognitive and psychomotor functioning during hangover revealed impairments in collective problem solving and response inhibition, but not attentional bias towards alcohol-related cues. The alcohol hangover state further significantly impaired driving performance, even for a short commute to work. With regard to the pathology of the alcohol hangover, research was presented that demonstrated increases in saliva cytokine concentrations confirming drinking alcohol and the hangover phase are both associated with an immune response. Other presentations discussed that scientific literature shows that there are no effective hangover treatments available yet. However, although promising, new hangover treatments are currently in development. Taken together, at the 10th Alcohol Hangover Research Group meeting, a comprehensive overview of the causes, consequences, and potential treatments of the alcohol hangover was presented.
Background
A number of social drinkers claim that they do not experience next-day hangovers despite consuming large quantities of alcohol. The aim of this study was to investigate the characteristics of drinkers who claim to be hangover immune and compare them with drinkers who do report having hangovers.
Methods
A total of 36 social drinkers participated in a naturalistic study consisting of a hangover day (alcohol consumed) and a control day (no alcohol consumed). Data were collected on alcohol consumption, demographics, sleep, next-day adverse effects, and mood. Data from drinkers with a hangover (N=18) were compared with data from drinkers who claim to be hangover immune (N=18).
Results
Drinkers with a hangover reported drowsiness-related symptoms, symptoms related to reduced cognitive functioning, and classic hangover symptoms such as headache, nausea, dizziness, weakness, and stomach pain. Corresponding mood changes comprised increased feelings of depression, anger–hostility, fatigue, and reduced vigor–activity. In contrast, hangover-immune drinkers reported relatively few hangover symptoms, with only mild corresponding severity scores. The reported symptoms were limited to drowsiness-related symptoms such as sleepiness and being tired. The classic hangover symptoms were usually not reported by these drinkers.
Conclusion
In contrast to drinkers with a hangover, for those who claim to be hangover immune, next-day adverse effects of alcohol consumption are limited to a mild increase in drowsiness-related symptoms.
Background:
The aim of this study was to examine the relationship between urine ethanol concentration and alcohol hangover severity.
Methods:
N = 36 healthy social drinkers participated in a naturalistic study, comprising a hangover day and a control day. N = 18 of them have regular hangovers (the hangover group), while the other N = 18 claim to be hangover immune (hangover-immune group). On each test day at 9.30 am, urine samples were collected. Participants rated their overall hangover severity on a scale from 0 (absent) to 10 (extreme), as well as 18 individual hangover symptoms.
Results:
Urine ethanol concentration was significantly higher on the hangover day when compared to the control day (p = 0.006). On the hangover day, urine ethanol concentration was significantly lower in the hangover-immune group when compared to the hangover group (p = 0.027). In the hangover-immune group, none of the correlations of urine ethanol concentration with individual hangover symptoms was significant. In contrast, in the hangover group, significant correlations were found with a variety of hangover symptoms, including nausea, concentration problems, sleepiness, weakness, apathy, sweating, stomach pain, thirst, heart racing, anxiety, and sleep problems.
Conclusion:
Urine ethanol levels are significantly associated with the presence and severity of several hangover symptoms.
Irritable bowel syndrome (IBS) is traditionally defined as a functional disorder since it lack of demonstrable pathological abnormalities. However, in recent years, low grade inflammatory infiltration, often rich in mast cells, in both the small and large bowel has been observed in some patients with IBS. The close association of mast cells with major intestinal functions, such as epithelial secretion and permeability, neuroimmune interactions, visceral sensation and peristalsis, makes researchers and gastroenterologists to focus attention on the key roles of mast cells in the pathogenesis of IBS. Numerous studies have been carried out to identify the mechanisms in the development, infiltration, activation and degranulation of intestinal mast cells, as well as the actions of mast cells in the processes of mucosal barrier disruption, mucosal immune dysregulation, visceral hypersensitivity, dysmotility, local and central stress in IBS. Moreover, therapies targeting mast cells, such as mast cell stabilizers (cromoglycate and ketotifen), antagonists of histamine and serotonin receptors, have been tried in IBS patients, and partly exhibited considerable efficacy. This review focuses on recent advances in the role of mast cells in IBS, with particular emphasis on bridging experimental data with clinical therapeutics for IBS patients.
Histamine is a biogenic amine with extensive effects on many cell types, mediated by the activation of its four receptors (H1R-H4R). Distinct effects are dependent on receptor subtypes and their differential expression. Within the gastrointestinal tract, histamine is present at relatively high concentrations, particularly during inflammatory responses. In this review, we discuss the immunoregulatory influence of histamine on a number of gastrointestinal disorders, including food allergy, scombroid food poisoning, histamine intolerance, irritable bowel syndrome, and inflammatory bowel disease. It is clear that the effects of histamine on mucosal immune homeostasis are dependent on expression and activity of the four currently known histamine receptors; however, the relative protective or pathogenic effects of histamine on inflammatory processes within the gut are still poorly defined and require further investigation.
Short-chain fatty acids (SCFAs) have been shown to promote intestinal barrier function, but their protective effects against ethanol-induced intestinal injury and underlying mechanisms remain essentially unknown. The aim of the study was to analyze the influence of SCFAs on ethanol-induced barrier dysfunction and to examine the role of AMP-activated protein kinase (AMPK) as a possible mechanism using Caco-2 monolayers. The monolayers were treated apically with butyrate (2, 10, or 20 mmol/L), propionate (4, 20, or 40 mmol/L), or acetate (8, 40, or 80 mmol/L) for 1 h before ethanol (40 mmol/L) for 3 h. Barrier function was analyzed by measurement of transepithelial resistance and permeation of fluorescein isothiocyanate-labeled dextran. Distribution of the tight junction (TJ) proteins zona occludens-1, occludin, and filamentous-actin (F-actin) was examined by immunofluorescence. Metabolic stress was determined by measuring oxidative stress, mitochondrial function, and ATP using dichlorofluorescein diacetate, dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide, and bioluminescence assay, respectively. AMPK was knocked down by small interfering RNA (siRNA), and its activity was assessed by a cell-based ELISA. Exposure to ethanol significantly impaired the barrier function compared with controls (P < 0.0001) and disrupted the TJ and F-actin cytoskeleton integrity and induction of metabolic stress. However, pretreatment with 2 mmol/L butyrate, 4 mmol/L propionate, and 8 mmol/L acetate significantly alleviated the ethanol-induced barrier dysfunction, TJ and F-actin disruption, as well as metabolic stress compared with ethanol-exposed monolayers (P < 0.0001). The promoting effects on barrier function were abolished by inhibiting AMPK using either compound C or siRNA. These observations indicate that SCFAs exhibit protective effects against ethanol-induced barrier disruption via AMPK activation, suggesting a potential for SCFAs as prophylactic and/or therapeutic factors against ethanol-induced gut leakiness.
Objective
This study aims to develop a new alcohol hangover symptom severity scale and compare its effectiveness with the Hangover Symptoms Scale (HSS), the Acute Hangover Scale (AHS), and a one-item hangover score.
Methods
Data from 1,410 Dutch students (Penning et al., Alcohol Alcohol 47:248-252, 2012) on the severity of 47 hangover symptoms were re-analyzed to develop the Alcohol Hangover Severity Scale (AHSS). The psychometric properties of the AHSS were compared with those of the HSS and the AHS. A survey among 1,000 students compared the AHSS and HSS with a one-item hangover severity score. The AHSS was further tested in a naturalistic hangover experiment.
Results
The 12 items of the AHSS were fatigue, clumsiness, dizziness, apathy, sweating, shivering, nausea, heart pounding, confusion, stomach pain, concentration problems, and thirst. The Penning et al. (Alcohol Alcohol 47:248–252, 2012) data revealed that the predictive validity of the AHSS (92.4 %) for the overall hangover score was significantly higher than that of the HSS (81.5 %) and the AHS (71.0 %). The survey data (N = 966) showed that scores on the AHSS (39.7 %) and the HSS (47.6 %) only moderately predicted the one-item hangover score. A total of 119 subjects completed the naturalistic study. On average, they consumed 9.7 alcoholic consumptions, yielding a mean estimated blood alcohol concentration (BAC) of 0.16 %. During hangover, the AHSS score correlated significantly with the number of alcoholic consumptions (r = 0.38, p < 0.0001) and estimated BAC (r = 0.40, p < 0.0001).
Conclusions
The AHS, HSS, and AHSS all seem appropriate for application in hangover research. The use of a one-item hangover scale is not recommended.
Intestinal barrier dysfunction and translocation of endotoxins are involved in the pathogenesis of alcoholic liver disease. Exposure to ethanol and its metabolite, acetaldehyde at relatively high concentrations have been shown to disrupt intestinal epithelial tight junctions in the conventional two dimensional cell culture models. The present study investigated quantitatively and qualitatively the effects of ethanol at concentrations detected in the blood after moderate ethanol consumption, of its metabolite acetaldehyde and of the combination of both compounds on intestinal barrier function in a three-dimensional cell culture model.
Caco-2 cells were grown in a basement membrane matrix (Matrigel™) to induce spheroid formation and were then exposed to the compounds at the basolateral side. Morphological differentiation of the spheroids was assessed by immunocytochemistry and transmission electron microscopy. The barrier function was assessed by the flux of FITC-labeled dextran from the basal side into the spheroids' luminal compartment using confocal microscopy. Caco-2 cells grown on Matrigel assembled into fully differentiated and polarized spheroids with a central lumen, closely resembling enterocytes in vivo and provide an excellent model to study epithelial barrier functionality. Exposure to ethanol (10-40 mM) or acetaldehyde (25-200 µM) for 3 h, dose-dependently and additively increased the paracellular permeability and induced redistribution of ZO-1 and occludin without affecting cell viability or tight junction-encoding gene expression. Furthermore, ethanol and acetaldehyde induced lysine residue and microtubules hyperacetylation.
These results indicate that ethanol at concentrations found in the blood after moderate drinking and acetaldehyde, alone and in combination, can increase the intestinal epithelial permeability. The data also point to the involvement of protein hyperacetylation in ethanol- and acetaldehyde-induced loss of tight junctions integrity.
Scientific literature suggests a large number of symptoms that may be present the day after excessive alcohol consumption. The purpose of this study was to explore the presence and severity of hangover symptoms, and determine their interrelationship.
A survey was conducted among n = 1410 Dutch students examining their drinking behavior and latest alcohol hangover. The severity of 47 presumed hangover symptoms were scored on a 10-point scale ranging from 0 (absent) to 10 (maximal). Factor analysis was conducted to summarize the data into groups of associated symptoms that contribute significantly to the alcohol hangover and symptoms that do not.
About half of the participants (56.1%, n = 791) reported having had a hangover during the past month. Most commonly reported and most severe hangover symptoms were fatigue (95.5%) and thirst (89.1%). Factor analysis revealed 11 factors that together account for 62% of variance. The most prominent factor 'drowsiness' (explained variance 28.8%) included symptoms such as drowsiness, fatigue, sleepiness and weakness. The second factor 'cognitive problems' (explained variance 5.9%) included symptoms such as reduced alertness, memory and concentration problems. Other factors, including the factor 'disturbed water balance' comprising frequently reported symptoms such as 'dry mouth' and 'thirst', contributed much less to the overall hangover (explained variance <5%).
Drowsiness and impaired cognitive functioning are the two dominant features of alcohol hangover.
Mainly known for its more famous parent compound, ethanol, acetaldehyde was first studied in the 1940s, but then research interest in this compound waned. However, in the last two decades, research on acetaldehyde has seen a revitalized and uninterrupted interest. Acetaldehyde, per se, and as a product of ethanol metabolism, is responsible for many pharmacological effects which are not clearly distinguishable from those of its parent compound, ethanol. Consequently, the most recent advances in acetaldehyde's psychopharmacology have been inspired by the experimental approach to test the hypothesis that some of the effects of ethanol are mediated by acetaldehyde and, in this regard, the characterization of metabolic pathways for ethanol and the localization within discrete brain regions of these effects have revitalized the interest on the role of acetaldehyde in ethanol's central effects. Here we present and discuss a wealth of experimental evidence that converges to suggest that acetaldehyde is an intrinsically active compound, is metabolically generated in the brain and, finally, mediates many of the psychopharmacological properties of ethanol.
The purpose of this study was to estimate the socioeconomic costs resulting from alcohol drinking among adolescents as of 2006 from a societal perspective.
The costs were classified into direct costs, indirect costs, and other costs. The direct costs consisted of direct medical costs and direct non-medical costs. The indirect costs were computed by future income losses from premature death, productivity losses from using medical services and reduction of productivity from drinking and hangover. The other costs consisted of property damage, public administrative expenses, and traffic accident compensation.
The socioeconomic costs of alcohol drinking among adolescents as of 2006 were estimated to be 387.5 billion won (0.05% of GDP). In the case of the former, the amount included 48.25% for reduction of productivity from drinking and hangover, 39.38% for future income losses from premature death, and 6.71% for hangover costs.
The results showed that the socioeconomic costs of alcohol drinking among adolescents in Korea were a serious as compared with that of the United States. Therefore, the active interventions such as a surveillance system and a prevention program to control adolescents drinking by government and preventive medicine specialist are needed.
The use of alcohol and drugs may affect workplace safety and productivity. Little is known about the magnitude of this problem in Norway.
Employee recruitment methods with or without individual follow-up were compared. The employees filled in a questionnaire and provided a sample of oral fluid. Samples were analysed for alcohol, ethyl glucuronide (EtG; a biological marker of recent large alcohol intake), psychoactive medicinal drugs and illegal drugs.
Participation rates with and without individual follow-up were 96% and 68%, respectively. Alcohol was negative (</=0.1 mg/ml) in all samples, but 21.0% reported the intake of alcohol during the last 24 h. EtG was positive (>2.2 ng/ml) in 2.1% of the samples. In-efficiency or hangover at work during the past year was reported by 24.3%, while 6.2% had been absent from work due to the use of alcohol. The combination of self-report and analytical testing indicated that medicinal or illegal drugs had been used during the last 48 h by 5.1% and 1.7% of the participants, respectively; while only 4.2% and 0.4% admitted the use in the questionnaire.
Self-reported data suggest that hangover after drinking alcohol appears to be the largest substance abuse problem at Norwegian workplaces, resulting in absence and inefficiency at work. Analysis of oral fluid revealed that the use of illegal drugs was more common than drinking alcohol before working or at the workplace. The analysis of oral fluid may be a valuable tool in obtaining additional information on alcohol and drug use compared to using questionnaires alone.
Alcohol and histamine metabolic pathways in the body have the common enzymes aldehyde dehydrogenase and aldehyde oxidase. The metabolite of ethanol, acetaldehyde, can effectively compete with the metabolites of histamine, methylimidazole acetaldehyde, and imidazole acetaldehyde. At the periphery, alcohol and acetaldehyde liberate histamine from its store in mast cells and depress histamine elimination by inhibiting diamine oxidase, resulting in elevated histamine levels in tissues. Histamine mediates alcohol-induced gastric and intestinal damage and bronchial asthma as well as flushing in Orientals. On the other hand, alcohol provokes food-induced histaminosis and histamine intolerance, which is an epidemiological problem. There are many controversial reports concerning the effect of H2 receptor antagonists on ethanol metabolism and the activity of alcohol dehydrogenase in the stomach. In addition, alcohol affects histamine levels in the brain by modulating histamine synthesis, release, and turnover. Histamine receptor antagonists can affect ethanol metabolism and change the sensitivity of animals to the hypnotic effects of alcohol. In contrast to other neurotransmitters, the involvement of the brain histamine system in the mechanisms of the central actions of alcohol and in the pathogenesis of alcoholism is poorly studied and understood.
Alcohol and the athlete have been linked together since ancient times. It continues to be the most commonly consumed drug among the athletic population. Alcohol use carries significant potential adverse effects for both the health and welfare of the individual. It is suggested that alcohol related problems may be more prevalent in the athletic population due to their risk taking mentality and the age profile of athletes (18- to 24-year-old males). Alcohol consumption also appears to have a causative effect in sports related injury, with an injury incidence of 54.8% in drinkers compared with 23.5% in nondrinkers (p < 0.005). This may be due in part to the hangover effect of alcohol consumption, which has been shown to reduce athletic performance by 11.4%. Alcohol is a potentially lethal drug and is a banned substance for certain Olympic sports. Education is the cornerstone for appropriate social use of this drug. Athletes and coaches need to be aware of the sports related adverse effects of alcohol consumption and its role in sports injury and poor physiological performance. It is recommended that alcohol should be avoided by the serious athlete.
The impairing effects on memory functioning after acute alcohol intoxication in healthy volunteers and after chronic use in alcoholics are well established. However, research determining the next-morning effects of a single episode of binge drinking on memory functioning is scarce. A total of 48 healthy volunteers participated in a single-blind study comprising an evening (baseline) session, followed by a treatment administration (ethanol 1.4 g/kg or placebo), and a morning session. Memory was tested with a word-learning test (including immediate and delayed recall, and recognition). Further, a 45-min Mackworth clock test for measuring vigilance was included (parameters: number of hits and false alarms) and subjective alertness was assessed, to infer whether word-learning test findings reflect sedation or specific memory impairments. Delayed recall in the morning session was significantly worse in the alcohol group when compared to the placebo group (F(1,42)=6.0, p<0.02). In contrast, immediate recall and recognition were unimpaired in the alcohol group. In the morning session, relative to the placebo group, subjective alertness was significantly reduced in the alcohol group before and after the tests (F(1,44)=8.7, p<0.005; F(1,44)=13.3, p&<0.001, respectively). However, in the Mackworth clock test, the alcohol group and placebo group did not differ significantly in the morning session. The specific findings of impaired delayed recall show that memory retrieval processes are significantly impaired during alcohol hangover. Vigilance performance was not significantly affected, indicating that this memory impairment does not reflect sedation.
Hangovers are a frequent, though unpleasant, experience among people who drink to intoxication. Despite the prevalence of hangovers, however, this condition is not well understood scientifically. Multiple possible contributors to the hangover state have been investigated, and researchers have produced evidence that alcohol can directly promote hangover symptoms through its effects on urine production, the gastrointestinal tract, blood sugar concentrations, sleep patterns, and biological rhythms. In addition, researchers postulate that effects related to alcohol's absence after a drinking bout (i.e., withdrawal), alcohol metabolism, and other factors (e.g., biologically active, nonalcohol compounds in beverages; the use of other drugs; certain personality traits; and a family history of alcoholism) also may contribute to the hangover condition. Few of the treatments commonly described for hangover have undergone scientific evaluation.
To assess the clinical evidence on the effectiveness of any medical intervention for preventing or treating alcohol hangover.
Systematic searches on Medline, Embase, Amed, Cochrane Central, the National Research Register (UK), and ClincalTrials.gov (USA); hand searches of conference proceedings and bibliographies; contact with experts and manufacturers of commercial preparations. Language of publication was not restricted.
All randomised controlled trials of any medical intervention for preventing or treating alcohol hangover were included. Trials were considered if they were placebo controlled or controlled against a comparator intervention. Titles and abstracts of identified articles were read and hard copies were obtained. The selection of studies, data extraction, and validation were done independently by two reviewers. The Jadad score was used to evaluate methodological quality.
Fifteen potentially relevant trials were identified. Seven publications failed to meet all inclusion criteria. Eight randomised controlled trials assessing eight different interventions were reviewed. The agents tested were propranolol, tropisetron, tolfenamic acid, fructose or glucose, and the dietary supplements Borago officinalis (borage), Cynara scolymus (artichoke), Opuntia ficus-indica (prickly pear), and a yeast based preparation. All studies were double blind. Significant intergroup differences for overall symptom scores and individual symptoms were reported only for tolfenamic acid, gamma linolenic acid from B officinalis, and a yeast based preparation.
No compelling evidence exists to suggest that any conventional or complementary intervention is effective for preventing or treating alcohol hangover. The most effective way to avoid the symptoms of alcohol induced hangover is to practise abstinence or moderation.
Objective:
Although much research has explored overall alcohol use in the workforce, little research has explored the extent of alcohol use and impairment in the workplace. This study explored the overall prevalence, frequency, and distribution of alcohol use and impairment during the workday.
Method:
Data were collected from a national probability sample of 2805 employed adults using a random digit dialing telephone survey. Alcohol use within 2 hours of reporting to work, alcohol use during the workday, working under the influence of alcohol, and working with a hangover were assessed for the 12 months preceding the interview.
Results:
Workplace alcohol use and impairment directly affect an estimated 15% of the U.S. workforce (19.2 million workers). Specifically, an estimated 1.83% (2.3 million workers) drink before work, 7.06% (8.9 million workers) drink during the workday, 1.68% (2.1 million workers) work under the influence of alcohol, and 9.23% (11.6 million workers) work with a hangover. The results also suggest that most workplace alcohol use and impairment occur infrequently. The distribution of workplace alcohol use and impairment differs by gender, race, age, marital status, occupation, and work shift.
Conclusion:
Workplace alcohol use and impairment are prevalent enough that additional research should focus on their causes and impact on employee productivity. Moreover, clear policies should be in place regarding alcohol use and impairment at work. But despite management's responsibility for the development and enforcement of such policies, managers report elevated rates of consuming alcohol during the workday, working under the influence of alcohol, and working with a hangover.
Decisions about using addictive substances are influenced by distractions by addiction-related stimuli, of which the user might be unaware. The addiction-Stroop task is a paradigm used to assess this distraction. The empirical evidence for the addiction-Stroop effect is critically reviewed, and meta-analyses of alcohol-related and smoking-related studies are presented. Studies finding the strongest effects were those in which participants had strong current concerns about an addictive substance or such concerns were highlighted through experimental manipulations, especially those depriving participants of the substance. Theories to account for addiction-related attentional bias are discussed, of which the motivational theory of current concerns appears to provide the most complete account of the phenomenon. Recommendations are made for maximizing the precision of the addiction-Stroop test in future research.
Histamine intolerance results from a disequilibrium of accumulated histamine and the capacity for histamine degradation. Histamine is a biogenic amine that occurs to various degrees in many foods. In healthy persons, dietary histamine can be rapidly detoxified by amine oxidases, whereas persons with low amine oxidase activity are at risk of histamine toxicity. Diamine oxidase (DAO) is the main enzyme for the metabolism of ingested histamine. It has been proposed that DAO, when functioning as a secretory protein, may be responsible for scavenging extracellular histamine after mediator release. Conversely, histamine N-methyltransferase, the other important enzyme inactivating histamine, is a cytosolic protein that can convert histamine only in the intracellular space of cells. An impaired histamine degradation based on reduced DAO activity and the resulting histamine excess may cause numerous symptoms mimicking an allergic reaction. The ingestion of histamine-rich food or of alcohol or drugs that release histamine or block DAO may provoke diarrhea, headache, rhinoconjunctival symptoms, asthma, hypotension, arrhythmia, urticaria, pruritus, flushing, and other conditions in patients with histamine intolerance. Symptoms can be reduced by a histamine-free diet or be eliminated by antihistamines. However, because of the multifaceted nature of the symptoms, the existence of histamine intolerance has been underestimated, and further studies based on double-blind, placebo-controlled provocations are needed. In patients in whom the abovementioned symptoms are triggered by the corresponding substances and who have a negative diagnosis of allergy or internal disorders, histamine intolerance should be considered as an underlying pathomechanism.
Up to now there is no adequate definition of the alcohol hangover. The purpose of the current study was to develop a useful definition, and consensus among those who will use it in scientific publications. A survey was conducted among N=1099 social drinkers who recently had a hangover. They were asked to provide their definition of the alcohol hangover. Text mining and content analysis revealed 3 potential definitions. These were submitted to members of the Alcohol Hangover Research Group, who were asked to give their expert opinion on the proposed definitions. Taking into account their comments and suggestions, the following definition for the alcohol hangover was formulated: "The alcohol hangover refers to the combination of cognitive and physical symptoms, experienced the day after a single episode of heavy drinking, starting when blood alcohol concentration approaches zero."
The findings obtained with the textual Stroop paradigm, testing for an attentional bias towards alcohol stimuli in heavier compared to lighter social drinkers, are limited in number and inconsistent in outcome. Using a pictorial rather than textual Stroop paradigm for the first time in alcohol research, a significant alcohol attentional bias is reported in heavier social drinkers compared to lighter social drinking controls. According to Cohen's scheme, the significant effect size is classified as ‘large'. The presence of an alcohol attentional bias helps to explain the perpetuation of abusive/dependent consumption and the frequency of post-treatment relapse. In a similar vein, these results add to the evidence that a differential alcohol attentional bias might also be present between two levels of social drinking and, in heavier social drinkers, has the potential to impact on the contents of awareness and the flow of thought towards alcohol. In this respect, it extends the small group of other perceptual-cognitive effects measured in social drinkers (alcohol cue reactions, alcohol associations and alcohol expectancies) that can influence the initiation of consumption in some social drinkers.
Effects of binge drinking on cognitive control and response selection are increasingly recognized in research on alcohol (ethanol) effects. Yet, little is known about how those processes are modulated by hangover effects.
Given that acute intoxication and hangover seem to be characterized by partly divergent effects and mechanisms, further research on this topic is needed. In the current study, we hence investigated this with a special focus on potentially differential effects of alcohol intoxication and subsequent hangover on sub-processes involved in the decision to select a response. We do so combining drift diffusion modelling of behavioral data with neurophysiological (EEG) data. Opposed to common sense, the results do not show an impairment of all assessed measures. Instead, they show specific effects of high dose alcohol intoxication and hangover on selective drift diffusion model and EEG parameters (as compared to a sober state). While the acute intoxication induced by binge-drinking decreased the drift rate, it was increased by the subsequent hangover, indicating more efficient information accumulation during hangover. Further, the nondecisional
processes of information encoding decreased with intoxication, but not during hangover. These effects were reflected in modulations of the N2, P1 and N1 event-related potentials, which reflect conflict monitoring,
perceptual gating and attentional selection processes, respectively. As regards the functional neuroanatomical architecture, the anterior cingulate cortex (ACC) as well as occipital networks seem to be modulated. Even
though alcohol is known to have broad neurobiological effects, its effects on cognitive processes are rather specific.
Introduction:
Excessive alcohol use cost the U.S. 249.0 billion in 2010, or about 100.7 billion (40.4%) of these costs. Binge drinking accounted for 24.3 billion (9.7%) of costs; and drinking while pregnant 3.5 billion. Binge drinking was responsible for >70% of these costs in all states, and >40% of the binge drinking-related costs were paid by government.
Conclusions:
Excessive drinking cost the nation almost 5 of the total cost was paid by government, and three quarters of the costs were due to binge drinking. Several evidence-based strategies can help reduce excessive drinking and related costs, including increasing alcohol excise taxes, limiting alcohol outlet density, and commercial host liability.
Difficulties in monitoring ongoing behaviour may be linked to real-life problematic drinking behaviours. Prior research suggests female heavy drinkers in particular display greater cognitive control deficits. Here, we examine trial-to-trial behavioural adaptations in a conflict monitoring task, relative to drinking behaviour and sex. Heavy drinkers (n=31, 16 male) and controls (n=35, 18 male) completed an Eriksen flanker task while brain electrical activity was recorded. For reaction time, error rates, and N2 and P3 amplitude of the event-related potential, trial-to-trial conflict adaptation was evidenced by a differential response to the current (congruent vs. incongruent) trials dependent on the identity of the previous trial. For the proportion of errors, heavy drinkers showed increased conflict adaptation compared to controls. Conflict adaptation for N2 (indexing monitoring) was larger for female heavy drinkers than controls, and the opposite was observed for males. There were no interactions involving group or sex for the P3 (indexing inhibition). The results suggest a compensatory response, such that heavy drinkers are required to increase performance monitoring in order to achieve the same behavioural outcome as controls. We also confirm the importance of sex as a factor in the relationship between behavioural control and heavy alcohol use.
Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
The aim of this study was to evaluate the effect of fexofenadine on intestinal inflammation. HCT116 and COLO205 cells were pretreated with fexofenadine and then stimulated with tumor necrosis factor (TNF)-α. Interleukin (IL)-8 expression was determined by real-time RT-PCR and ELISA. DNA binding activity of NF-κB was assessed by electrophoretic mobility shift assay. The molecular markers of endoplasmic reticulum (ER) stress were evaluated by Western blot analysis and PCR. In the acute colitis model, mice were given 4% dextran sulfate sodium (DSS) for 5 days with or without fexofenadine. IL-10-/- mice were used to evaluate the effect of fexofenadine on chronic colitis. Fexofenadine significantly inhibited the upregulated expression of IL-8 in HCT116 and COLO205 cells stimulated with TNF-α. Fexofenadine suppressed NF-κB DNA binding activity. CHOP mRNA expression was enhanced in the presence of TNF-α, and it was dampened by pretreatment of fexofenadine. In addition, the induction of ER stress markers caspase-12 and p-eIF2-α were significantly suppressed by the pretreatment of fexofenadine. Administration of fexofenadine significantly reduced the severity of DSS-induced murine colitis, as assessed by the disease activity index, colon length, and histology. In addition, the DSS-induced phospho-IKK activation was significantly decreased in fexofenadine-pretreated mice. Finally, fexofenadine significantly reduced the severity of colitis and the immunoreactivity of caspase-12 and p-eIF2-α in IL-10 -/- mice as compared with controls. These results suggest that fexofenadine is a potential therapeutic agent for the treatment of inflammatory bowel disease.
The American Society for Pharmacology and Experimental Therapeutics.
Objectives:
Alcohol hangover may impair potentially dangerous daily activities such as driving a car or operating heavy machinery. The purpose of the present study was to determine (1) whether driving during alcohol hangover is a problem of concern among professional Dutch truck drivers and (2) to what extent they think their hangover state affects driving performance.
Methods:
Three hundred forty-three professional truck drivers were interviewed at a Dutch trucker festival. In addition to demographics, data were gathered on normal driving, alcohol consumption and hangover, and driving style during alcohol hangover.
Results:
More than half of the professional drivers who consume alcohol and report occasionally having a hangover (56.4%) acknowledge that they have driven while having a hangover during the past year: 26.5 percent only when driving private, 2.6 percent only when driving professionally, and 27.4 percent both private and professionally. Additionally, 45.3 percent reported driving while having a hangover sometimes, whereas 7.7 percent and 1.7 percent reported doing so often or always, respectively. During alcohol hangover, professional drivers rated their driving style as significantly less relaxed, less safe, and less responsible (P < .001).
Conclusions:
Driving with a hangover is a common phenomenon, and professional drivers acknowledge that their driving is impaired. Therefore, future experimental research should examine the magnitude of impairment while driving with an alcohol hangover.
Recent electrophysiological evidence suggests that ethanol simultaneously exerts opposite effects on the activity of dopamine (DA) neurons in the ventral tegmental area (VTA) through two parallel mechanisms, one promoting and the other reducing the GABA release onto VTA DA neurons. Here we explore the possible behavioural implications of these findings by investigating the role displayed by acetaldehyde (the main metabolite of ethanol) and the non-metabolized fraction of ethanol in motor activity of rats. We analyse the appearance of motor activation or depression after intra-VTA administration of ethanol in rats subjected to different pharmacological pre-treatments designed to preferentially test either the effects of acetaldehyde or the non-metabolized ethanol. Motor activity was evaluated after intra-VTA administration of 35 nmol of ethanol, an apparently ineffective dose that does not modify the motor activity of animals. Pharmacological pre-treatments were used in order to either increase (cyanamide, 10 mg/kg, ip) or decrease (D-penicillamine, 50 mg/kg, ip and sodium azide, 7 mg/kg, ip) acetaldehyde levels in the VTA. Pre-treatments aimed to augment acetaldehyde, increased motor activity of rats. Otherwise, pre-treatments intended to decrease local acetaldehyde levels evoked significant reductions in motor activity that were prevented by the local blockade (bicuculline, 17.5 pmol) of the GABAA receptors. Our findings suggest that the brain-generated acetaldehyde is involved in the stimulant effects of ethanol, whereas the non-biotransformed fraction of ethanol, acting through the GABAA receptors, would account for the depressant effects. The present behavioural findings suggest that ethanol dually modulates the activity of DA neurons.
PurposeThe purpose of this study was to validate the Dutch version of the Brief Young Adult Alcohol Consequences Questionnaire (B-YAACQ).
Research on human subjects analyzing blood and urine samples determined biological correlates that may explain the pathology of alcohol hangover. These analyses showed that concentrations of various hormones, electrolytes, free fatty acids, triglycerides, lactate, ketone bodies, cortisol, and glucose were not significantly correlated with reported alcohol hangover severity. Also, markers of dehydration (e.g., vasopressin) were not significantly related to hangover severity. Some studies report a significant correlation between blood acetaldehyde concentration and hangover severity, but most convincing is the significant relationship between immune factors and hangover severity. The latter is supported by studies showing that hangover severity may be reduced by inhibitors of prostaglandin synthesis. Several factors do not cause alcohol hangover but can aggravate its severity. These include sleep deprivation, smoking, congeners, health status, genetics and individual differences. Future studies should more rigorously study these factors as well as biological correlates to further elucidate the pathology of alcohol hangover.
The search for alcohol hangover cures is as old as alcohol itself. Many cures and prophylactic agents are available, but scientific evidence for their effectiveness is generally lacking. This review summarizes and discusses the limited number of studies that examined the effectiveness of alcohol hangover treatments. From these studies it must be concluded that most remedies do not significantly reduce overall hangover severity. Some compounds reduce specific symptoms such as vomiting and headache, but are not effective in reducing other common hangover symptoms such as drowsiness and fatigue. Hangover cures that showed positive effects were those inhibiting prostaglandin synthesis or accelerating alcohol metabolism. Future studies should elucidate the pathology of alcohol hangover. Until then, it is unlikely that an effective hangover cure will be developed.
There has been a great deal of activity in recent years in the study of the direct effects of ethanol on the dopamine reward system originating in the ventral tegmental area (VTA). In addition, recent evidence suggests that acetaldehyde formed from ethanol in the brain or periphery may be a crucial factor in the central effects of ethanol. This critical review examines the actions of ethanol and acetaldehyde on neurons of the VTA and the possible interactions with stress, with a focus on electrophysiological studies in vivo and in vitro. Ethanol has specific effects on dopamine neurons and there is recent evidence that some of the in vivo and in vitro effects of ethanol are mediated by acetaldehyde. Stress has some analogous actions on neuronal activity in the VTA, and the interactions between the effects of stress and alcohol on VTA neurons may be a factor in ethanol-seeking behavior. Taken together, the evidence suggests that stress may contribute to the activating effects of ethanol on dopamine VTA neurons, that at least some actions of ethanol on dopamine VTA neurons are mediated by acetaldehyde, and that the interaction between stress and alcohol could play a role in susceptibility to alcoholism. The link between acetaldehyde and ethanol actions on brain reward pathways may provide a new avenue for the development of agents to reduce alcohol craving.
The gut may prime inflammatory responses following shock/trauma insults. Ethanol (EtOH) use is common in trauma patients and may impair intestinal barrier function. We compared varying concentrations of EtOH on proinflammatory cytokine production of Caco2 cell monolayers and the resultant changes in barrier function. We hypothesized that even low concentrations of EtOH would cause significant cytokine release and barrier dysfunction in vitro.
Confluent Caco2 cell monolayers were grown in a two-chamber culture system and exposed to varying concentrations of EtOH (0.1%, 0.5%, 1.0%, 1.5%, and 2.0%) with/without Escherichia coli C-25 (EC). Supernatants were collected and TNF and IL6 quantified by ELISA (pg/mL). Monolayer integrity was assessed by apoptosis and permeability measurements.
Caco2 production of TNF-alpha increased in a dose-dependent manner when incubated with increasing concentrations of EtoH. A synergistic effect was seen when E. coli was added to the apical chamber. A similar result was seen with the production of IL-6. A dose-dependent effect was also noted with EtOH with or without E. coli on apoptosis and permeability measurements.
In addition to alterations in gut permeability, increasing concentrations of ethanol have a synergistic effect with E. coli on Caco2 production of proinflammatory cytokines TNF and IL-6. The creation of a proinflammatory cytokine milieu with an altered barrier integrity may be a mechanism by which ethanol may increase septic complications in the injured patient.
The EEG was recorded in 27 subjects during hangover. Male healthy volunteers drank 1.75 g/kg body weight of ethanol in 3 h and the EEG was recorded 14-16 h later when the degree of hangover was highest. For control purposes a second EEG was recorded after a similar session when subjects drank water instead of ethanol. A third record was taken in normal laboratory conditions. T5-A1 and O1-A1 derivations were subjected to computer analysis from which spectral and frequency parameters were calculated. Visual analysis of the EEG during hangover showed a decrease and slowing of alpha activity and an increase in theta activity. Spectral analysis of the EEG gave a statistically significant increase in 7-8 c/sec activity during hangover. The EEG change could not be explained in terms of blood alcohol level, hypoglycaemia or acidosis. Also fatigue could be excluded as a cause of EEG change by means of "water controls". The conclusion is that the slowing of the EEG during hangover is caused by the depressant action of ethanol, or its metabolites, on cortical function.
The role of several metabolic and endocrine factors in the pathogenesis of hangover has been studied in healthy human volunteers under experimental conditions. Significant changes in the blood concentrations of acetaldehyde, glucose, lactate, ketone bodies and free fatty acids were found during hangover, but none of these changes correlated with the intensity of hangover. Plasma electrolyte concentrations were not changed during hangover, except for a mild metabolic acidosis which had a significant correlation with the intensity of hangover. The metabolic changes, including acidosis, could be prevented by the administration of fructose. However, fructose had no effect on the intensity of hangover. The basal concentrations of the anterior-pituitary hormones, i. e., thyroid stimulating hormone (TSH), luteinizing hormone (LH), growth hormone (GH) and prolactin (PRL), in plasma were not significantly altered during hangover. The secretion of TSH and LH induced by the administration of the releasing hormones (TRH and LHRH) was not affected by alcohol intoxication or hangover, but the TRH-induced release of PRL was totally blocked during hangover. This may indicate increased dopaminergic activity in the hypothalamus during hangover. The plasma concentration of Cortisol was elevated and that of testosterone decreased during hangover, but these changes are probably only unspecific reactions to the stress. It is concluded that the metabolic and endocrine factors studied by us probably do not have any major role in the pathogenesis of hangover. However, the observed changes in the secretion of PRL may reflect the primary neural events involved in the induction of hangover.
Auditory evoked responses (AER) to trains of 6 click stimuli (1 click/sec) were studied in 9 subjects under hangover, tired control, and normal control conditions in order to find out whether the symptoms of hyperexcitability during hangover have a correlate in the characteristics of the AER. In addition, the audiograms were measured. AERs to the first click in a stimulus train were markedly smaller during hangover than in the other 2 states. The amplitude levels of the AERs during the repetition of the click stimulus were, however, similar under all three conditions. The audiograms obtained in the three states were similar except for a very slight decrease of auditory threshold sensitivity during hangover as compared with the tired control condition. The results show that the effects of hangover on AERs resemble those of alcohol intoxication. The symptoms of hyperexcitability during hangover cannot be explained in terms of increased peripheral sensitivity.
The effects of alcohols on the formation of leukotrienes, 5-HETE and prostaglandin D2 in mastocytoma cells and human neutrophils were studied. In murine mastocytoma cells, alcohols appear to have at least two different effects on the production of these arachidonic acid metabolites. At low levels of cellular arachidonic acid achieved after stimulation with calcium ionophore A23187 or addition of low levels of exogenous arachidonic acid, alcohols appear to have a general inhibitory effect on the production of lipoxygenase metabolites. In the presence of higher concentrations of cellular arachidonic acid, ethanol and methanol stimulated the production of lipoxygenase metabolites, but had no large stimulatory effect on the cyclo-oxygenase metabolite, prostaglandin D2. Under these conditions, n-propanol and t-butanol have inhibitory effects on leukotriene production. Human neutrophils are less sensitive to ethanol than mastocytoma cells, but stimulatory effects were still found at high ethanol concentrations (220-430 mM).
This study examined the time-course of alcohol impairment of general aviation pilot simulator performance. We tested 14 young (mean age 25.8 years) and 14 older (mean age 37.9 years) pilots in a Frasca 141 simulator during alcohol and placebo conditions. In the alcohol condition, pilots drank alcohol and were tested after reaching 0.10% BAL, and then 2, 4, 8, 24, and 48 h after they had stopped drinking. They were tested at the same times in the placebo condition. Alcohol impaired overall performance. Alcohol impairment also depended on the order in which subjects participated in the alcohol and placebo sessions, with larger decrements for the alcohol-placebo order than for the opposite order. To examine the influence of alcohol independent of session order effects, we compared performance in the first alcohol session with performance in the first placebo session. This analysis showed that alcohol significantly reduced mean performance in the alcohol condition at 0.10% BAL and at 2 h. In addition, alcohol increased variability in performance in the alcohol session from 0.10% BAL to 8 h, suggesting that some subjects were more susceptible to alcohol than others. Older pilots tended to perform some radio communication tasks less accurately than younger pilots.
Alcohol consumption is known to be associated with both risk of accidental injury and with sensation seeking, and sensation seeking has been found to be common among those engaging in such high-risk activities as skiing. However, few studies have examined the joint association of alcohol consumption and sensation seeking on injury.
Alcohol consumption prior to injury and sensation-seeking disposition are analyzed on 389 injured skiers (clinic sample) and 899 randomly selected uninjured skiers (trailside sample) at a Northeastern ski resort. Cases and controls were asked questions pertaining to drinking within 24 hours, amount consumed, time lapsed between the last drink and the event, skiing ability, and sensation seeking.
The clinic sample was more likely to be female, to have less skiing experience, to score lower on sensation seeking and to have been drinking within 24 hours compared to the trailside sample. However, they were less likely to have had six or more drinks within 24 hours and were more likely to report a greater time lapse between the last drink and injury or interview. A larger proportion of those who reported drinking in both samples scored high on sensation seeking compared to those who reported not drinking. Logistic regression analysis found the following variables predictive of ski injury: female, low on sensation seeking, amount of alcohol consumed prior to the event, a longer time lapsed between drinking and the event, time of day (later) and day of the week (weekend).
The data suggest that, while drinking within 24 hours is positively associated with sensation seeking, drinking and not sensation seeking is positively predictive of injury. Drinking at least 12 hours prior to skiing, not drinking in close proximity to skiing, may increase risk for accidental injury, possibly due to a hangover or residual alcohol effect in which fatigue may play a part.
Carry-over effects or the hangover hypothesis postulates that alcohol continues to impair performance the morning after drinking, even after low or moderate doses. Performance deficits have been attributed to the residual effects of recent drinking. The present study examined evidence for residual alcohol consumption on human performance when blood alcohol level has declined to zero.
A within-subjects, repeated measures, placebo controlled experiment was conducted with double-blind alcohol administration to investigate the effects of alcohol the morning after ingestion.
All subjects were studied in Glasgow, Scotland, UK.
Forty healthy male moderate to heavy social drinkers between 18 and 45 years of age.
Psychomotor performance, subjective state and quality of sleep were examined under alcohol and placebo with a 1-week interval between test sessions. Enough alcohol was given to place subjects above the legal limit for driving at peak blood alcohol.
There was no evidence for impaired performance the morning after ingestion. Effects were found for subjective state and sleep quality.
The findings suggest that after a 100 mg/100 ml dose of alcohol people who: (a) have no alcohol left in their blood and; (b) do not feel hung over will generally be fit to drive.
A hangover is the syndrome of physical and mental symptoms that occurs 8 to 16 h after alcohol consumption with a zero level of alcohol. The aim of the current study was to investigate the effects of the alcohol hangover on cytokine production in healthy subjects. The hangover state was defined as 13 h after drinking 1.5 g/kg of alcohol (blood alcohol level=0). A venous blood sample was taken from 20 healthy adult men before consumption of alcohol and during the hangover state. Peripheral blood mononuclear cells were separated and stimulated with phytohemagglutinin. An enzyme-linked immunosorbent assay was used to measure the production of the following cytokines: interleukin (IL)-1beta, IL-4, IL-6, IL-10, IL-12, interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha). We found that the concentrations of IL-10, IL-12, and IFN-gamma were significantly increased during the hangover state compared with the concentrations in normal conditions. These results support the suggestion that the dysregulated cytokine pathway (IL-10, IL-12, and IFN-gamma) is associated with the symptoms of hangovers.
One hypothesis concerning the human dorsal anterior cingulate cortex (ACC) is that it functions, in part, to signal the occurrence of conflicts in information processing, thereby triggering compensatory adjustments in cognitive control. Since this idea was first proposed, a great deal of relevant empirical evidence has accrued. This evidence has largely corroborated the conflict-monitoring hypothesis, and some very recent work has provided striking new support for the theory. At the same time, other findings have posed specific challenges, especially concerning the way the theory addresses the processing of errors. Recent research has also begun to shed light on the larger function of the ACC, suggesting some new possibilities concerning how conflict monitoring might fit into the cingulate's overall role in cognition and action.
To investigate the effects of students' usual levels of alcohol consumption on aspects of mood and anxiety the following morning.
Students were recruited who consumed their usual quantity of any type of alcoholic beverage in their chosen company and then completed assessments of the effects the following day. The timing of drinking was restricted to the period between 22:00 and 02:00 h the night before testing as these are the most popular hours for consuming alcohol in the population under investigation. The testing included an assessment of mood and anxiety; testing was also performed after an evening of abstinence (no hangover condition), following a counterbalanced repeated measure design, with time of testing and order of testing as 'between participant' factors. Forty-eight student social drinkers (33 women, 15 men) aged between 18 and 43 years were tested, with a 1 week interval between test sessions.
Males reported consuming on average 14.7 units and females 10.5 units the night before testing. On the morning after alcohol consumption, ratings of alertness and tranquility were lower than the ratings the morning following an evening of abstinence at both 11:00 and 13:00 h and the post intoxication physical symptoms, emotional symptoms and symptoms of fatigue persisted throughout the morning.
Heavy alcohol consumption lowers mood, disrupts sleep, increases anxiety and produces physical symptoms, emotional symptoms and symptoms of fatigue throughout the next morning.
Little research has examined antecedents of specific drinking consequences (vomiting, regretted sex, hangover, blackouts) among college students. This research examined how students' experiences of past consequences relate to their beliefs of experiencing similar consequences in the future and how these beliefs relate to current drinking patterns.
Self-reported past drinking behavior and resulting consequences associated with specific occasions were assessed among 303 (66% women) college students. Students also estimated number of drinks associated with risk of experiencing future similar consequences.
Paired-samples t tests indicated that students significantly overestimated the number of drinks it would take to vomit, have unwanted sexual experiences, experience hangovers, and black out in comparison with the actual self-reported number of drinks consumed the last time identical consequences were experienced. In addition, a series of multiple-regression analyses revealed that greater misperceptions between the perceived and actual number of drinks associated with each type of consequence were consistently associated with heavier drinking.
Results suggest that heavier-drinking students do not learn from their mistakes but instead overestimate the amount of alcohol they can consume without experiencing negative consequences. Clinical implications of these findings are discussed in terms of augmenting brief interventions aimed at heavy-drinking college students.
To investigate immunomodulatory properties of 4 antihistamines available in Japan.
Isolated peripheral blood T cells from healthy volunteers were preincubated with cetirizine, loratadine, olopatadine, or fexofenadine for 30 minutes and then stimulated with interleukin (IL)-1 2 or IL-4 to skew immune response towards type 1 or type 2 helper T cells. RNA was extracted 6 hours later and semiquantitative reverse transcription polymerase chain reaction (RT-PCR) was performed using primers for IL-5 and interferon (IFN) gamma. Supernatants were collected 24 hours after stimulation, and cytokine production was quantified by enzyme-linked immunosorbent assay (ELISA).
RT-PCR revealed that IL-12-induced expression of IFN-gamma was partially suppressed by loratadine and fexofenadine and that all 4 agents tested inhibited IL-4-induced expression of IL-5. ELISA demonstrated that IL-12-induced IFN-gamma production was significantly suppressed by cetirizine and fexofenadine and IL-4-induced IL-5 production was downregulated by three agents with the exception of cetirizine. This study demonstrates that antihistamines have varying immunomodulatory properties, suggesting treatment choice for atopic dermatitis can be directed by disease signs and symptoms.
Alcohol hangover is characterized by adverse physical and mental effects that occur the next morning after the intake of toxic doses of alcohol. One of the more relevant functional consequences of hangover is the cognitive and subjective impairment, which could be related to the high socioeconomic costs of alcohol consumption. Nevertheless, few studies have addressed the study of neurocognitive and subjective effects of hangover. The systematic and exhaustive study of neurocognitive and subjective effects has not been done. In the present work we briefly review the hangover impact, not only in the objective execution of attention, psychomotricity and memory tasks, but in the subjective state of the subjects as well. Moreover, we also highlight the methodology difficulties to study neurocognitive effects of hangover and suggest several aspects to take into account in future investigations.
The alcohol hangover develops when blood alcohol concentration (BAC) returns to zero and is characterized by a feeling of general misery that may last more than 24 h. It comprises a variety of symptoms including drowsiness, concentration problems, dry mouth, dizziness, gastro-intestinal complaints, sweating, nausea, hyper-excitability, and anxiety. The alcohol hangover is an intriguing issue since it is unknown why these symptoms are present after alcohol and its metabolites are eliminated from the body. Although numerous scientific papers cover the acute effects of alcohol consumption, researchers largely neglected the issue of alcohol hangover. This lack of scientific interest is remarkable, since almost everybody is familiar with the unpleasant hangover effects that may arise the day after an evening of excessive drinking, and with the ways these symptoms may affect performance of planned activities.
- Department
- Health
Department of Health. Social Services & Public Safety: Available
from: https://www.hesa.ac.uk/data-and-analysis/publications/ highereducation-2014-15/introduction (accessed on 2014).
Acute and hangover effects of alcohol on event-related poten-tials (erps)
- A Fox
- C Nabke
- G Chesher
- J Greeley
- J Lemon
Fox A, Nabke C, Chesher G, Greeley J, Lemon J. Acute and
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International Conference on Alcohol, Drugs and Traffic Safety-T92, Proceedings of the 12 th Conference.