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News Article | May 4, 2017
Site: www.winespectator.com

Just like your brain after a night of excessive drinking, the science behind hangovers is a little fuzzy Many of us like to believe we're well past our days of waking up feeling a bit wooly, but the fact is, hangovers can happen to the best of us—and to add injury to insult, they get worse with age. So if you had too much bubbly at a party, or one glass more of Merlot proved to be one glass too many, what do you do to combat the headache, nausea, fatigue and shakiness that might afflict you the following day? For ancient Romans, the "best" way to recover after a wild bacchanal was to eat fried canary for breakfast. According to Irish legend, burying yourself in wet river sand will ease your head after too many pints. Medieval European overindulgers believed consuming raw eel could counteract the effects of too much booze-driven merriment. You may scoff at these remedies, but how much better are our modern-day day-after rituals? There's not a lot of science-backed information about hangovers—we still don't even know why we get them. And if we can't pinpoint the cause, how can we expect to have a cure? "Nobody knows what causes it," Jonathan Howland, professor at Boston University and director of the injury prevention center at Boston Medical Center told Wine Spectator. "So to say that you're going to cure a hangover, or prevent a hangover, or you're just going to magically take care of all the symptoms, well, that's maybe stretching it a bit." But don't lose hope. Just because there's no proven end-all be-all antidote for your post-wine woes, there are still some proven methods for feeling better. "There are various things that can treat symptoms of hangover that are perfectly legitimate," Howland said. Water is at the top of the list for anyone looking to treat a hangover. "Lots of water, and my personal favorite, coconut water—loaded with electrolytes—can help the issue of dehydration and really make us feel better," said registered dietician Isabel Smith via email. But while rehydrating is important, especially after a long night of alcohol, studies suggest that dehydration is just one reason we feel so bad after drinking too much. Hangovers are caused by different reactions as our bodies process alcohol—a lot of the effects we feel while hungover are due to dehydration, but even if we are hydrated, there are plenty of other factors. So while you absolutely should drink lots of water after a night on the town, don't expect to make a miraculous recovery because of it. OK, so what about the harder stuff? "Does the hair of the dog work? It does, actually, but that is probably the worst possible thing you can do," said Thomas Kash, associate professor at the University of North Carolina Bowles Center for Alcohol Studies. It's well-known that a bloody mary at brunch might make you feel better temporarily, dulling the pain, but it's only prolonging the inevitable, and could leave you with a worse hangover than the one you were trying to get rid of. Kash and his fellow researchers also stress that a prolonged pattern of drinking to avoid hangovers can lead to dangerous habits. If you can't imbibe away your hangover pain, what about eating? Many hungover folks indulge in fatty foods, believing it soaks up the alcohol. Unfortunately, research suggests this is a myth. According to the Alcohol Hangover Research Group, a coalition of international researchers, hangovers develop as your blood-alcohol concentration is dropping. So if you're hungover, there's not really any alcohol present in the stomach for the food to soak up. So why do people think this method helps? "It could be that they were just hungry," Kash said. "They have a headache, they're tired, they feel kind of sick, but they're hungry on top of it." According to Damaris Rohsenow, associate director of the Center for Alcohol and Addiction Studies at Brown University, many researchers cite inflammation, brought on by different factors like the presence of congeners in the alcohol you drink or the release of chemicals in the body called cytokines, as a key cause of hangovers. So if you pop anti-inflammatory painkillers when you have a raging hangover headache, you may be getting straight to the source of the matter. But remember, not all over-the-counter painkillers are created equally. Acetaminophen, for example, is processed in the liver, so taking it after overdoing alcohol can cause serious damage. Aspirin and ibuprofen are considered safer, but you should never exceed the recommended dosage, since there is still a small risk of damaging the stomach lining. And wait until the morning after to take them—if you take them before bed after a night of drinking, not only is there a higher risk of damage (since there's still alcohol in your system), but it's also likely you'll still be asleep when the painkillers reach their peak effectiveness. What about those miracle pills advertised? Quick-fix products like Blowfish—an FDA-approved tablet that claims to "make you feel like a human again" with its formula of aspirin and caffeine—have made headlines in recent years. But just like all of the aforementioned tactics, researchers insist that these "cures" will only address a few symptoms, and each person will respond to them differently. While science may not have a silver bullet for hangovers, that hasn't stopped people from selling remedies. And there may be partial merit to some of them. A new trend in hangover treatment has been popping up in party cities like Las Vegas, Miami, New York and London: Intravenous hydration therapy. "Doctors, nurses, firefighters, people in the military have been using IV therapy long before it's been available to the general public," said Johnny Parvani, emergency-room physician and CEO of Reviv, a medical spa that provides non-emergency IV treatments. Not only does IV therapy help you rehydrate, but it could also directly address another possible cause for hangovers. "Ultimately, alcohol is converted into carbon dioxide and water, but the intermediaries between the alcohol and the final end product are some toxic metabolites," said Parvani. "Fluids are the most effective way of flushing all of these things out." It could put a spring back in your step—if you're willing to shell out between $99 to $300. Those who prefer to "sweat it out" with exercise (and elicit eye-rolls from their less athletically inclined peers) are encouraged to do so, but with caution. "Sweating a little bit sometimes can make you feel better," said New York–based wellness coach Danielle Pashko. "Through sweat you excrete toxins. But I wouldn't tell somebody to go for a run if they're not feeling up to it. If you're not feeling well, you could do a leisurely walk or something easy." And if you do choose to exercise, make sure you're drinking a lot of water to stay hydrated. "I think there's probably not a miracle cure out there," Kash said. And there may never be, he adds, since medical research tends to focus on more pressing matters than your aching head after a night of Prosecco. "People are more concerned with binge drinking and heavy alcohol dependency." Unfortunately for our Sunday morning selves, there doesn't seem to be a real hangover "cure" out there, just different ways to cope with the symptoms. So if you want to stay indoors all day and order pizza, go for it. If you'd rather pump vitamins into your bloodstream and then run a few miles, more power to you. As long as you stay hydrated and listen to your body—and remember that the only real way to avoid a hangover is to drink in moderation—do what feels best for you. It should only last a few hours, anyway.


Hayes D.M.,University of North Carolina at Chapel Hill | Fee J.R.,University of North Carolina at Chapel Hill | McCown T.J.,Gene Therapy Center | Knapp D.J.,Bowles Center for Alcohol Studies | And 10 more authors.
Addiction Biology | Year: 2012

Neuropeptide Y (NPY) and protein kinase A (PKA) have been implicated in neurobiological responses to ethanol. We have previously reported that mutant mice lacking normal production of the RIIβ subunit of PKA (RIIβ-/- mice) show enhanced sensitivity to the locomotor stimulant effects of ethanol and increased behavioral sensitization relative to littermate wild-type RIIβ+/+ mice. We now report that RIIβ-/- mice also show increased NPY immunoreactivity in the nucleus accumbens (NAc) core and the ventral striatum relative to RIIβ+/+ mice. These observations suggest that elevated NPY signaling in the NAc and/or striatum may contribute to the increased sensitivity to ethanol-induced behavioral sensitization that is a characteristic of RIIβ-/- mice. Consistently, NPY-/- mice failed to display ethanol-induced behavioral sensitization that was evident in littermate NPY+/+ mice. To examine more directly the role of NPY in the locomotor stimulant effects of ethanol, we infused a recombinant adeno-associated virus (rAAV) into the region of the NAc core of DBA/2J mice. The rAAV-fibronectin (FIB)-NPY 13-36 vector expresses and constitutively secretes the NPY fragment NPY 13-36 (a selective Y 2 receptor agonist) from infected cells in vivo. Mice treated with the rAAV-FIB-NPY 13-36 vector exhibited reduced expression of ethanol-induced behavioral sensitization compared with mice treated with a control vector. Taken together, the current data provide the first evidence that NPY signaling in the NAc core and the Y 2 receptor modulate ethanol-induced behavioral sensitization. © 2011 Society for the Study of Addiction.


Berger L.,University of Wisconsin - Milwaukee | Brondino M.,University of Wisconsin - Milwaukee | Gwyther R.,Bowles Center for Alcohol Studies | Garbutt J.C.,Bowles Center for Alcohol Studies | Garbutt J.C.,University of North Carolina at Chapel Hill
Journal of the American Board of Family Medicine | Year: 2016

Background: In a recent study conducted in a family medicine setting, the medication acamprosate was found not to be efficacious in the treatment of alcohol dependence, but a drinking goal of abstinence was found to have positive effects on alcohol use outcomes. The purpose of this secondary analysis was to further understand which patients with an alcohol use disorder may be most successfully treated in a primary care setting. Methods: The study was exploratory and used a trajectory-based approach based on data from the acamprosate treatment trial of 100 participants (recruited mostly by advertisement) who were randomly assigned to receive either acamprosate or a matching placebo. Post hoc trajectories of alcohol use before treatment were identified to examine whether trajectory classes and their interactions with treatment arm (acamprosate or placebo), pretreatment drinking goal (abstinence or a reduction), and time predicted alcohol use outcomes. Results: Three distinct trajectory classes were identified: frequent drinkers, nearly daily drinkers, and consistent daily drinkers. Consistent daily drinkers with a goal of abstinence significantly improved over time on the primary outcome measure of percent days abstinent when compared with frequent and nearly daily drinkers. In addition, all participants with a goal of abstinence, regardless of trajectory class, significantly reduced their percentage of heavy drinking days over time. Conclusions: Patients with an alcohol use disorder who have a drinking goal of abstinence, in particular consistent daily drinkers, may maximally benefit from alcohol use disorder treatment, including the use of medication, in a primary care setting.


PubMed | CB and 7175 and Bowles Center for Alcohol Studies
Type: Journal Article | Journal: Psychopharmacology | Year: 2016

Anxiety during pregnancy has been linked to adverse maternal health outcomes, including postpartum depression (PPD). However, there has been limited study of biological mechanisms underlying behavioral predictors of PPD during pregnancy.Considering the shared etiology of chronic stress amongst antenatal behavioral predictors, the primary goal of this pilot study was to examine associations among stress-related physiological factors (including GABA-ergic neurosteroids) and stress-related behavioral indices of anxiety during pregnancy.Fourteen nulliparous women in their second trimester of a singleton pregnancy underwent speech and mental arithmetic stress, following a 2-week subjective and objective recording of sleep-wake behavior.Lower cortisol, progesterone, and a combined measure of ALLO+pregnanolone throughout the entire stressor protocol (area under the curve, AUC) were associated with greater negative emotional responses to stress, and lower cortisol AUC was associated with worse sleep quality. Lower adrenocorticotropic hormone was associated with greater anxious and depressive symptoms. Stress produced paradoxical reductions in cortisol, progesterone, and a combined measure of allopregnanolone+pregnanolone, while tetrahydrodeoxycorticosterone levels were elevated.These data suggest that cortisol, progesterone, and ALLO+pregnanolone levels in the second trimester of pregnancy are inversely related to negative emotional symptoms, and the negative impact of acute stress challenge appears to exert its effects by reducing these steroids to further promote negative emotional responses.


Fish E.W.,University of North Carolina at Chapel Hill | Fish E.W.,Bowles Center for Alcohol Studies | Agoglia A.E.,Bowles Center for Alcohol Studies | Agoglia A.E.,University of North Carolina at Chapel Hill | And 8 more authors.
Behavioural Pharmacology | Year: 2014

The antiepileptic levetiracetam (LEV) has been investigated for the treatment of alcohol abuse. However, little is known about how LEV alters the behavioral effects of alcohol in laboratory animals. The acute effects of LEV on alcohol drinking by male C57BL/6J mice were investigated using two different drinking procedures, limited access [drinking-in-the-dark (DID)] and intermittent access (IA) drinking. In the first experiment (DID), mice had access to a single bottle containing alcohol or sucrose for 4 h every other day. In the second experiment (IA), mice had IA to two bottles, one containing alcohol or sucrose and one containing water, for 24 h on Monday, Wednesday, and Friday. In both experiments, mice were administered LEV (0.3-100 mg/kg intraperitoneally) or vehicle 30 min before access to the drinking solutions. In the DID mice, LEV increased alcohol intake from 4.3 to 5.4 g/kg, whereas in the IA mice LEV decreased alcohol intake from 4.8 to 3.0 g/kg in the first 4 h of access and decreased 24 h alcohol intake from 20 to ∼15 g/kg. These effects appear specific to alcohol, as LEV did not affect sucrose intake in either experiment. LEV appears to differentially affect drinking in animal models of moderate and heavier alcohol consumption. © 2014 Wolters Kluwer Health.


Lovinger D.M.,U.S. National Institutes of Health | Kash T.L.,Bowles Center for Alcohol Studies
Alcohol research : current reviews | Year: 2015

Long-lasting changes in synaptic function (i.e., synaptic plasticity) have long been thought to contribute to information storage in the nervous system. Although synaptic plasticity mainly has adaptive functions that allow the organism to function in complex environments, it is now clear that certain events or exposure to various substances can produce plasticity that has negative consequences for organisms. Exposure to drugs of abuse, in particular ethanol, is a life experience that can activate or alter synaptic plasticity, often resulting in increased drug seeking and taking and in many cases addiction.Two brain regions subject to alcohol's effects on synaptic plasticity are the striatum and bed nucleus of the stria terminalis (BNST), both of which have key roles in alcohol's actions and control of intake. The specific effects depend on both the brain region analyzed (e.g., specific subregions of the striatum and BNST) and the duration of ethanol exposure (i.e., acute vs. chronic). Plastic changes in synaptic transmission in these two brain regions following prolonged ethanol exposure are thought to contribute to excessive alcohol drinking and relapse to drinking. Understanding the mechanisms underlying this plasticity may lead to new therapies for treatment of these and other aspects of alcohol use disorder.


Oguz I.,University of North Carolina at Chapel Hill | Lee J.,UNC | Budin F.,University of North Carolina at Chapel Hill | Rumple A.,University of North Carolina at Chapel Hill | And 5 more authors.
Progress in Biomedical Optics and Imaging - Proceedings of SPIE | Year: 2011

3D Magnetic Resonance (MR) and Diffusion Tensor Imaging (DTI) have become important noninvasive tools for the study of animal models of brain development and neuropathologies. Fully automated analysis methods adapted to rodent scale for these images will allow highthroughput studies. A fundamental first step for most quantitative analysis algorithms is skullstripping, which refers to the segmentation of the image into two tissue categories, brain and non-brain. In this manuscript, we present a fully automatic skull-stripping algorithm in an atlasbased manner. We also demonstrate how to either modify an external atlas or to build an atlas from the population itself to present a self-contained approach. We applied our method to three datasets of rat brain scans, at different ages (PND5, PND14 and adult), different study groups (control, ethanol exposed, intrauterine cocaine exposed), as well as different image acquisition parameters. We validated our method by comparing the automated skull-strip results to manual delineations performed by our expert, which showed a discrepancy of less than a single voxel on average. We thus demonstrate that our algorithm can robustly and accurately perform the skull-stripping within one voxel of the manual delineation, and in a fraction of the time it takes a human expert. © 2011 Copyright Society of Photo-Optical Instrumentation Engineers (SPIE).


Huang M.M.,Bowles Center for Alcohol Studies | Overstreet D.H.,Bowles Center for Alcohol Studies | Overstreet D.H.,University of North Carolina at Chapel Hill | Knapp D.J.,Bowles Center for Alcohol Studies | And 9 more authors.
Journal of Pharmacology and Experimental Therapeutics | Year: 2010

In abstinent alcoholics, stress induces negative affect - a response linked to craving and relapse. In rats, repeated stresses at weekly intervals before 5-day ethanol diet sensitize withdrawalinduced anxiety-like behavior ("anxiety") that is blocked by a corticotrophin-releasing factor 1 (CRF-1)-receptor antagonist. Current experiments were performed to identify brain sites that support CRF involvement in stress sensitization of ethanol withdrawal-induced anxiety-like behavior. First, different doses of CRF microinjected weekly into the central amygdala (CeA) before ethanol exposure produced a dose-related sensitization of anxiety during ethanol withdrawal. Subsequently, CRF microinjection into the basolateral amygdala, dorsal raphe nucleus (DRN), or dorsal bed nucleus of the stria terminalis (d-BNST) also sensitized ethanol withdrawal-induced anxiety. In contrast, sensitization of ethanol withdrawal-induced anxiety was not observed after weekly CRF administration into the ventral-BNST, CA1-hippocampal region, or hypothalamic-paraventricular nucleus. Then, experiments documented the CRF receptor subtype responsible for CRF and stress sensitization of withdrawal-induced anxiety. Systemic administration of a CRF-1 receptor antagonist before CRF microinjection into the CeA, DRN, or d-BNST prevented CRF-induced sensitization of anxiety during ethanol withdrawal. Furthermore, repeated microinjections of urocortin-3, a CRF-2 receptor agonist, into the CRF-positive sites did not sensitize anxiety after withdrawal from ethanol. Finally, microinjection of a CRF-1 receptor antagonist into the CeA, DRN, or d-BNST before stress blocked sensitization of anxiety-like behavior induced by the repeated stress/ethanol withdrawal protocol. These results indicate that CRF released by stress acts on CRF-1 receptors within specific brain regions to produce a cumulative adaptation that sensitizes anxiety-like behavior during withdrawal from chronic ethanol exposure. Copyright © 2010 by The American Society for Pharmacology and Experimental Therapeutics.


PubMed | University of North Carolina at Chapel Hill and Bowles Center for Alcohol Studies
Type: | Journal: Neuropharmacology | Year: 2015

Gabapentin, a drug used in the treatment of epileptic seizures and neuropathic pain, has shown efficacy in the treatment of alcohol dependence. Moreover, given that gabapentin is used in the general population (e.g., non-dependent individuals, social drinkers), we sought to utilize preclinical assessments to examine the effects of gabapentin on sensitivity to moderate alcohol doses and alcohol self-administration in rats with a history of moderate drinking. To this end, we assessed whether gabapentin (0, 10, 30, 120 mg/kg, IG) pretreatment alters sensitivity to experimenter- and self-administered alcohol, and whether gabapentin alone has alcohol-like discriminative stimulus effects in rats trained to discriminate alcohol dose (1 g/kg, IG) vs. water. Second, we assessed whether gabapentin (0, 10, 30, 60 mg/kg, IG) would alter alcohol self-administration. Gabapentin pretreatment potentiated the interoceptive effects of both experimenter-administered and self-administered alcohol in discrimination-trained rats. Additionally, the highest gabapentin doses tested (30 and 120 mg/kg) were found to have partial alcohol-like discriminative stimulus effects when administered alone (e.g., without alcohol). In the self-administration trained rats, gabapentin pretreatment (60 mg/kg) resulted in an escalation in alcohol self-administration. Given the importance of interoceptive drug cues in priming and maintaining self-administration, these data define a specific behavioral mechanism (i.e., potentiation of alcohol effects) by which gabapentin may increase alcohol self-administration in non-dependent populations.


PubMed | Bowles Center for Alcohol Studies
Type: | Journal: Journal of neuroinflammation | Year: 2012

Activation of microglia causes the production of proinflammatory factors and upregulation of NADPH oxidase (NOX) that form reactive oxygen species (ROS) that lead to neurodegeneration. Previously, we reported that 10 daily doses of ethanol treatment induced innate immune genes in brain. In the present study, we investigate the effects of chronic ethanol on activation of NOX and release of ROS, and their contribution to ethanol neurotoxicity.Male C57BL/6 and NF-B enhanced GFP mice were treated intragastrically with water or ethanol (5 g/kg, i.g., 25% ethanol w/v) daily for 10 days. The effects of chronic ethanol on cell death markers (activated caspase-3 and Fluoro-Jade B), microglial morphology, NOX, ROS and NF-B were examined using real-time PCR, immunohistochemistry and hydroethidine histochemistry. Also, Fluoro-Jade B staining and NOX gp91phox immunohistochemistry were performed in the orbitofrontal cortex (OFC) of human postmortem alcoholic brain and human moderate drinking control brain.Ethanol treatment of C57BL/6 mice showed increased markers of neuronal death: activated caspase-3 and Fluoro-Jade B positive staining with Neu-N (a neuronal marker) labeling in cortex and dentate gyrus. The OFC of human post-mortem alcoholic brain also showed significantly more Fluoro-Jade B positive cells colocalized with Neu-N, a neuronal marker, compared to the OFC of human moderate drinking control brain, suggesting increased neuronal death in the OFC of human alcoholic brain. Iba1 and GFAP immunohistochemistry showed activated morphology of microglia and astrocytes in ethanol-treated mouse brain. Ethanol treatment increased NF-B transcription and increased NOX gp91phox at 24 hr after the last ethanol treatment that remained elevated at 1 week. The OFC of human postmortem alcoholic brain also had significant increases in the number of gp91phox + immunoreactive (IR) cells that are colocalized with neuronal, microglial and astrocyte markers. In mouse brain ethanol increased gp91phox expression coincided with increased production of O2- and O2- - derived oxidants. Diphenyleneiodonium (DPI), a NOX inhibitor, reduced markers of neurodegeneration, ROS and microglial activation.Ethanol activation of microglia and astrocytes, induction of NOX and production of ROS contribute to chronic ethanol-induced neurotoxicity. NOX-ROS and NF-B signaling pathways play important roles in chronic ethanol-induced neuroinflammation and neurodegeneration.

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