Hangover Headache Research Articles

Hangover headache and its behavioral changes in rats.

The present study aims to establish and evaluate a rat model for hangover headaches caused by alcoholic drinks. 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). 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. 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.

ZBiotics raises funds for hangover probiotic

San Francisco–based ZBiotics has raised $2.3 million in seed funding from the venture capital firm Oyster Ventures. ZBiotics has engineered Bacillus subtilis to make acetaldehyde dehydrogenase, an enzyme that breaks down acetaldehyde, which some studies have linked to the hangover headache. The product is sold online. ZBiotics says the funds will help it scale up the hangover treatment and develop new engineered probiotics.

Alcoholic beverages as trigger factor and the effect on alcohol consumption behavior in patients with migraine.

Alcoholic beverages are frequently reported migraine triggers. We aimed to assess self-reported alcohol consumption as a migraine attack trigger and to investigate the effect on alcohol consumption behavior in a large migraine cohort. We conducted a cross-sectional, web-based, questionnaire study among 2197 patients with migraine from the well-defined Leiden University MIgraine Neuro-Analysis (LUMINA) study population. We assessed alcoholic beverage consumption and self-reported trigger potential, reasons behind alcohol abstinence and time between alcohol consumption and migraine attack onset. Alcoholic beverages were reported as a trigger by 35.6% of participants with migraine. In addition, over 25% of patients with migraine who had stopped consuming or never consumed alcoholic beverages did so because of presumed trigger effects. Wine, especially red wine (77.8% of participants), was recognized as the most common trigger among the alcoholic beverages. However, red wine consistently led to an attack in only 8.8% of participants. Time of onset was rapid (<3h) in one-third of patients and almost 90% had an onset <10h independent of beverage type. Alcoholic beverages, especially red wine, are recognized as a migraine trigger factor by patients with migraine and have a substantial effect on alcohol consumption behavior. Rapid onset of provoked migraine attacks in contrast to what is known about hangover headache might point to a different mechanism. The low consistency of provocation suggests that alcoholic beverages acting as a singular trigger is insufficient and may depend on a fluctuating trigger threshold.

The use of tomato aminoaldehyde dehydrogenase 1 for the detection of aldehydes in fruit distillates

Plant NAD(+)-dependent aminoaldehyde dehydrogenases (AMADHs, EC 1.2.1.19) belong to the family 10 of aldehyde dehydrogenases. They participate in the metabolism of polyamines or osmoprotectants. The enzymes are characterized by their broad substrate specificity covering ω-aminoaldehydes, aliphatic and aromatic aldehydes as well as nitrogen-containing heterocyclic aldehydes. The isoenzyme 1 from tomato (Solanum lycopersicum; SlAMADH1) oxidizes aliphatic aldehydes very efficiently and converts also furfural, its derivatives or benzaldehyde, which are present at low concentrations in alcoholic distillates such as fruit brandy. In this work, SlAMADH1 was examined as a bioanalytical tool for their detection. These aldehydes arise from fermentation processes or thermal degradation of sugars and their presence is related to health complications after consumption including nausea, emesis, sweating, decrease in blood pressure, hangover headache, among others. Sixteen samples of slivovitz (plum brandy) from local producers in Moravia, Czech Republic, were analyzed for their aldehyde content using a spectrophotometric activity assay with SlAMADH1. In all cases, there were oxidative responses observed when monitoring NADH production in the enzymatic reaction. Aldehydes in the distillate samples were also subjected to a standard determination using reversed-phase HPLC with spectrophotometric and tandem mass spectrometric detection after a derivatization with 2,4-dinitrophenylhydrazine. Results obtained by both methods were found to correlate well for a majority of the analyzed samples. The possible applicability of SlAMADH1 for the evaluation of aldehyde content in food and beverages has now been demonstrated.

Headache and Alcohol

The notion that alcohol intake may trigger headache is well known. Historical data as well as clinical experience indicate that this may be the case for headache patients as well persons without known headache disorders. This monograph reviews the medical literature about alcohol as a headache trigger, what headache types are triggered, and why. Literature search primarily using the terms "alcohol and headache," "migraine and alcohol," "cluster headache and alcohol," and "alcohol hangover headache," as well as combined search, was performed, limiting the search to the last decade. Relevant articles were picked. The search "alcohol and headache" yielded 918 hits for the decade 2004-2014. Combined search gave substantially less, and 30 papers were reviewed, of which 25 are included in this review. Epidemiological studies find some correlations between alcohol intake and mainly primary headache disorders, such as migraine and cluster headache. Cultural differences in alcohol consumption are probably reflected in some of the results and conclusions. Both migraine and cluster headaches may be triggered by alcohol; however, which type of alcoholic beverage triggers these headaches is not clear. There is no single mechanism that explains the pathophysiology of alcohol-induced headache, other that hangover headache in some may be triggered by inactive alcohol dehydrogenase 2. Alcohol-induced headache may be diagnosed as a secondary headache, while in patients with migraine or cluster headache alcohol intake may act as a trigger for these primary headaches. Based on the literature, there is no reason to tell headache patients in general to abstain from alcohol. Individual dispositions as well as cultural factors may play a role in alcohol-induced headache.

Cytological and Histological Effect of Paracetamol on the Testis and Liver in Albino Mice Mus musculus

The purpose of this study is to evaluate the acute toxicity effects of pure paracetamol tablets&#x0D; on laboratory mice. In this study Mus musculus mice (6-8) weeks old were used. The toxicity effects&#x0D; were evaluated on fifteen mice, in which they were divided equally into three groups, each one&#x0D; consists of five individual mice. The first group was labeled as a vehicle group and received 5mL/kg&#x0D; DW. The second and third groups were labeled as experimental groups which received 2 g/kg and 5&#x0D; g/kg of paracetamol respectively. After fifteen days the animals were examined for toxicity signs and&#x0D; then the liver and testis were processed for histological examinations. Furthermore, the sperm&#x0D; abnormalities were recorded. The results of this study demonstrated that the low dose did not show&#x0D; any morphological changes while some changes such as shivering, nausea and mortality were&#x0D; manifested after administration of high dose of paracetamol. Many histological changes have been&#x0D; observed after high dose treatment of paracetamol, the frequencies of abnormal sperm were&#x0D; increased as well. Therefore, Paracetamol, which is believed to be a strong pain killer for the&#x0D; hangover headache may damage liver and testis when consumes beyond the recommended dose.

Headache and wine. Are all wines the same?

Methods Based in previous data we have designed a simple and structured questionnaire. All patients attending a headache clinic (one day/week) during 6 months have been required to fill it. Age, gender, headache type (IHC-2004 criteria) are recorded. Questions referring to usual intake of wine, wine producing headache, kind of wine (red/white/sweet/ cava-champagne) were asked. Questions about other alcoholic beverages producing headache and hangover headache also were presented. In this paper we describe the Results.

Glucuronic acid and the ethanol metabolite ethyl-glucuronide cause toll-like receptor 4 activation and enhanced pain

We have previously observed that the non-opioid morphine metabolite, morphine-3-glucuronide, enhances pain via a toll-like receptor 4 (TLR4) dependent mechanism. The present studies were undertaken to determine whether TLR4-dependent pain enhancement generalizes to other classes of glucuronide metabolites. In silico modeling predicted that glucuronic acid alone and ethyl glucuronide, a minor but long-lasting ethanol metabolite, would dock to the same MD-2 portion of the TLR4 receptor complex previously characterized as the docking site for morphine-3-glucuronide. Glucuronic acid, ethyl glucuronide and ethanol all caused an increase in TLR4-dependent reporter protein expression in a cell line transfected with TLR4 and associated co-signaling molecules. Glucuronic acid-, ethyl glucuronide-, and ethanol-induced increases in TLR4 signaling were blocked by the TLR4 antagonists LPS-RS and (+)-naloxone. Glucuronic acid and ethyl glucuronide both caused allodynia following intrathecal injection in rats, which was blocked by intrathecal co-administration of the TLR4 antagonist LPS-RS. The finding that ethyl glucuronide can cause TLR4-dependent pain could have implications for human conditions such as hangover headache and alcohol withdrawal hyperalgesia, as well as suggesting that other classes of glucuronide metabolites could have similar effects.

Acetate causes alcohol hangover headache in rats.

BackgroundThe mechanism of veisalgia cephalgia or hangover headache is unknown. Despite a lack of mechanistic studies, there are a number of theories positing congeners, dehydration, or the ethanol metabolite acetaldehyde as causes of hangover headache.MethodsWe used a chronic headache model to examine how pure ethanol produces increased sensitivity for nociceptive behaviors in normally hydrated rats.ResultsEthanol initially decreased sensitivity to mechanical stimuli on the face (analgesia), followed 4 to 6 hours later by inflammatory pain. Inhibiting alcohol dehydrogenase extended the analgesia whereas inhibiting aldehyde dehydrogenase decreased analgesia. Neither treatment had nociceptive effects. Direct administration of acetate increased nociceptive behaviors suggesting that acetate, not acetaldehyde, accumulation results in hangover-like hypersensitivity in our model. Since adenosine accumulation is a result of acetate formation, we administered an adenosine antagonist that blocked hypersensitivity.DiscussionOur study shows that acetate contributes to hangover headache. These findings provide insight into the mechanism of hangover headache and the mechanism of headache induction.

Hangover headache: accompanying symptoms. Vågå study of headache epidemiology

As part of the Vågå study of headache epidemiology, the symptomatology of hangover headache has been studied in 1122 parishioners in the age group 18–65 years; male/female ratio 1.14. The following criteria for hangover headache were adhered to: (1) intoxication by alcohol, (2) headache, and (3) onset of headache >3 hours after discontinuation of drinking. As demonstrated elsewhere, headache was present in 64% of the cases. Throbbing was present in 85% of those affected, nausea in 60% and vomiting in 25%, with significant male preponderance for all three. Photo- and phonophobia were more rarely present. Not only does hangover headache seem to be more frequent in males—as previously demonstrated; it also seems to be more severe in males. Ninety per cent of the hangover headache victims felt that the gastro-intestinal symptoms originated in the gastro-intestinal tract and were not secondary to the headache.

Hangover headache: various manifestations and proposal for criteria. Vågå study of headache epidemiology

Hangover headache has been focused upon in connection with the Vågå study of headache epidemiology, with 714 cases among 1122 dalesmen (64%). Most frequently the headache was global in location. It was more frequently located in the anterior (frontotemporal) than occipital area. A unilateral headache was present in only 3% of the dalesmen, many of whom were migraineurs. Headache seemed to be more intense in males than females. Headache usually seemed to be of a lower intensity than the pain of migraine, but higher than, or similar to, that of tension-type headache. The headache appeared late in the night/early morning hours, i. e., several hours after discontinuation of drinking. In most cases, headache stopped in the late morning hours, or at high noon, but it could even last until somewhat late in the afternoon; it rarely, if ever, exceeded 12 hours duration. Red wine seemed mostly to provoke headache the same evening (with traits similar to those of the spontaneously occurring headache attacks). Criteria for hangover headache are proposed.

Hangover headache. Prevalence: Vågå study of headache epidemiology

In Vågå, Norway, with 3907 inhabitants, there were 2075 18–65-year-old dalesmen available for the headache epidemiology study. A total of 1838 dalesmen (88.6%) were personally examined. However, due to uncertainty whether hangover headache could be incorporated, this part of the study was started at no. 500. Of the remaining 1338 dalesmen, 1122, i. e., 83.9%, were questioned about hangover headache. The parochial “drinking culture” could probably best be characterised as binge drinking and not as a constant, daily consumption. Inclusion criteria were: intoxication by alcohol; headache; and the headache manifesting itself more than three hours after the end of drinking. In the whole series, 714 dalesmen had experienced hangover headache (“delayed alcohol-induced headache”) during their lifetime (64%). This may be the best way to express hangover headache prevalence. Among those who had been “exposed to proper amounts of alcohol”, the prevalence was considerably higher: 88%. With the existing drinking pattern, hangover headache clearly dominated in males (M/F ratio: 1.50 vs. 0.72 in those without hangover headache (p<0.0005)). Consistency tests showed high Kappa values.

New in neurology

Around 5000 delegates gathered in London, UK on 17–22 June 2001 for the twelfth World Congress of Neurology. The congress covered a diverse range of issues, from the shortage of neurologists in the UK to revealing a genetic component to migraine and clues to the hangover headache. New results were revealed in the fight against bovine spongiform encephalopathy (BSE) and Creutzfeldt-Jakob disease (CJD), and electrical impulse therapy was discussed as a new way to control epilepsy. The event was sponsored by The World Federation of Neurology, The Association of British Neurologists and The European Federation of Neurological Societies. KP

The True Story of Max and Moritz: Ancient and Medieval Texts before W. Busch

Wilhelm Busch (1832-1908) was a German cartoonist and poet whose most famous work was an illustrated dogtrot verse about a pair of little hellions called Max and Moritz. Published in German in 1865, it has delighted generations of German children and their parents and was eventually translated into English by editor and litterateur Christopher Morley in 1932. Knowledge of the Max and Moritz saga had come to Americans earlier, however, through the comic strip “The Katzenjammer Kids” (later “The Captain and the Kids”), first drawn by Rudolph Dirks for the New York Journal in 1897 and long continuing in popularity. (I remember a version of the cartoon in the 1930s as my own childhood favorite Sunday reading.) Katzenjammer is German for a ‘hangover headache’ (literally “cat’s clamoring”), which is presumably what the terrible twosome gave all the adults around them. Manfred Gorlach has continued and much expanded the Max and Moritz corpus by orchestrating the “discovery” for an overexpanding number of versions of the poem in many languages. The present volume brings together fragments and complete versions of the poem, which consists of a preface, seven tricks, and a conclusion. The fragments are from Egyptian, Sahidic, Ancient Greek, Umbarian, Latin, Gothic (in both Moeso and Crimean versions), Old High German, Old Saxon, Old West Norse, early Welsh, early Middle English (in Peterborough and Pershore versions), Anglo-Norman, Old Spanish, Medieval Latin, Middle Dutch, and others. The full text appears in Old English, Middle High German, late Middle English (Chaucerian), Middle Scots, and early Modern English, as well as the Busch recension and a contemporary English translation. The burden of this tongue-in-cheek scholarly display of textual analysis, iconographic description, manuscript history, and critical appraisal is that Wilhelm Busch was not, after all, the author of Max und Moritz but only a latter-day transmitter. Manfred Gorlach’s labor of love in creating this elaborately extensive spoof of linguistic analysis and textual criticism should earn him a special Nobel Prize for

Symptomatic and nonsymptomatic headaches in a general population.

We assessed the lifetime prevalences of headache disorders in a cross-sectional epidemiologic survey of a representative 25- to 64-year-old general population. We classified the headaches on the basis of a clinical interview and a physical and neurologic examination using the operational diagnostic criteria of the International Headache Society. Lifetime prevalence of idiopathic stabbing headache was 2%, of external compression headache 4%, and of cold stimulus headache 15%. Benign cough headache, benign exertional headache, and headache associated with sexual activity each occurred in 1%. Lifetime prevalence of hangover headache was 72%, of fever headache 63%, and of headache associated with disorders of nose or sinuses 15%. Headaches associated with severe structural lesions were rare. External compression headache, fever headache, headache associated with metabolic disorders, and headache associated with disorders of nose or sinuses all showed significant female preponderance. The symptomatic headaches and headaches unassociated with structural lesions were more prevalent among migraineurs. In subjects with tension-type headache, only hangover headache was overrepresented. There was no association between the headache disorders and abnormal routine blood chemistry or arterial hypertension. In women with migraine, however, diastolic blood pressure was significantly higher than in women without migraine.