Acute Alcohol Intake Research Articles

Rhubarb extract prevents hepatic inflammation induced by acute alcohol intake, an effect related to the modulation of the gut microbiota.

Binge consumption of alcohol is an alarming global health problem. Acute ethanol intoxication is characterized by hepatic inflammation and oxidative stress, which could be promoted by gut barrier function alterations. In this study, we have tested the hypothesis of the hepatoprotective effect of rhubarb extract in a mouse model of binge drinking and we explored the contribution of the gut microbiota in the related metabolic effects. Mice were fed a control diet supplemented with or without 0.3% rhubarb extract for 17 days and were necropsied 6 h after an alcohol challenge. Supplementation with rhubarb extract changed the microbial ecosystem (assessed by 16S rDNA pyrosequencing) in favor of Akkermansia muciniphila and Parabacteroides goldsteinii. Furthermore, it improved alcohol-induced hepatic injury, downregulated key markers of both inflammatory and oxidative stresses in the liver tissue, without affecting significantly steatosis. In the gut, rhubarb supplementation increased crypt depth, tissue weight, and the expression of antimicrobial peptides. These findings suggest that some bacterial genders involved in gut barrier function, are promoted by phytochemicals present in rhubarb extract, and could therefore be involved in the modulation of the susceptibility to hepatic diseases linked to acute alcohol consumption.

Alternative sampling strategies for the assessment of alcohol intake of living persons

Monitoring of alcohol consumption by living persons takes place in various contexts, amongst which workplace drug testing, driving under the influence of alcohol, driving licence regranting programs, alcohol withdrawal treatment, diagnosis of acute intoxication or fetal alcohol ingestion. The matrices that are mostly used today include blood, breath and urine. The aim of this review is to present alternative sampling strategies that allow monitoring of the alcohol consumption in living subjects. Ethanol itself, indirect (carbohydrate deficient transferrin, CDT%) as well as direct biomarkers (ethyl glucuronide, EtG; ethyl sulphate, EtS; fatty acid ethyl esters, FAEEs and phosphatidylethanol species, PEths) of ethanol consumption will be considered. This review covers dried blood spots (CDT%, EtG/EtS, PEths), dried urine spots (EtG/EtS), sweat and skin surface lipids (ethanol, EtG, FAEEs), oral fluid (ethanol, EtG), exhaled breath (PEths), hair (EtG, FAEEs), nail (EtG), meconium (EtG/EtS, FAEEs), umbilical cord and placenta (EtG/EtS and PEth 16:0/18:1). Main results, issues and considerations specific to each matrix are reported. Details about sample preparation and analytical methods are not within the scope of this review.

URB597 inhibits oxidative stress induced by alcohol binging in the prefrontal cortex of adolescent rats

Heavy episodic drinking (binging), which is highly prevalent among teenagers, results in oxidative damage. Because the prefrontal cortex (PFC) is not completely mature in adolescents, this brain region may be more vulnerable to the effects of alcohol during adolescence. As endocannabinoids may protect the immature PFC from the harmful effects of high doses of alcohol, this study investigated the effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597 on oxidative stress induced by acute or chronic binge alcohol intake in adolescent rats. At 40min after intraperitoneal pre-treatment with URB597 (0.3mg/kg) or vehicle (Veh), ethanol (EtOH; 3 or 6g/kg, intragastrically) or distilled water (DW) was administered in 3 consecutive sessions (acute binging) or 3 consecutive sessions over 4 weeks (chronic binging). Oxidative stress in PFC slices in situ was measured by dihydroethidium fluorescence staining. At the higher EtOH dose (6g/kg), pre-treatment with URB597 significantly reduced (p<0.01) the production of superoxide anions in the PFC after acute (42.8% decrease) and chronic binge EtOH consumption (44.9% decrease) compared with pre-treatment with Veh. As URB597 decreases anandamide metabolism, this evidence shows an antioxidant effect of endocannabinoids to suppress acute and chronic binge alcohol intake-induced oxidative stress in the PFC of adolescent rats.

Effect Of Acute Alcohol Ingestion On Resistance Exercise-Induced Muscle MTORC1 Signaling In Women.

Effect Of Acute Alcohol Ingestion On Resistance Exercise-Induced Muscle MTORC1 Signaling In Women.

Ethanol impedes embryo transport and impairs oviduct epithelium.

Most studies have demonstrated that alcohol consumption is associated with decreased fertility. The aim of this study was to investigate the effects of alcohol on pre-implantation embryo transport and/or early embryo development in the oviduct. We reported here that ethanol concentration-dependently suppressed the spontaneous motility of isolated human oviduct strips (EC50 50±6mM), which was largely attenuated in the present of L-NAME, a classical nitric oxide synthase(NOS) competitive inhibitor. Notably, either acute or chronic alcohol intake delayed egg transport and retarded early development of the embryo in the mouse oviduct, which was largely rescued by co-administration of L-NAME in a acute alcohol intake group but not in chronic alcohol intake group. It is worth mentioning that the oviductal epithelium destruction was verified by scanning electron microscope (SEM) observations in chronic alcohol intake group. In conclusion, alcohol intake delayed egg transport and retarded early development of the embryo in the oviduct by suppressing the spontaneous motility of oviduct and/or impairing oviductal epithelium. These findings suggested that alcohol abuse increases the incident of ectopic pregnancy.

Alcohol-related breast cancer in postmenopausal women - effect of CYP19A1, PPARG and PPARGC1A polymorphisms on female sex-hormone levels and interaction with alcohol consumption and NSAID usage in a nested case-control study and a randomised controlled trial.

BackgroundAlcohol consumption is associated with increased risk of breast cancer (BC), and the underlying mechanism is thought to be sex-hormone driven. In vitro and observational studies suggest a mechanism involving peroxisome proliferator-activated receptor gamma (PPARγ) in a complex with peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α) and interaction with aromatase (encoded by CYP19A1). Use of non-steroidal anti-inflammatory drugs (NSAID) may also affect circulating sex-hormone levels by modifying PPARγ activity.MethodsIn the present study we assessed whether genetic variation in CYP19A1 is associated with risk of BC in a case-control study group nested within the Danish “Diet, Cancer and Health” cohort (ncases = 687 and ncontrols = 687) and searched for gene-gene interaction between CYP19A1 and PPARGC1A, and CYP19A1 and PPARG, and gene-alcohol and gene-NSAID interactions. Association between the CYP19A1 polymorphisms and hormone levels was also examined among 339 non-HRT users. Incidence rate ratios were calculated based on Cox’ proportional hazards model. Furthermore, we performed a pilot randomised controlled trial to determine the effect of the PPARG Pro12Ala polymorphism and the PPARγ stimulator Ibuprofen on sex-hormone levels following alcohol intake in postmenopausal women (n = 25) using linear regression.ResultsGenetic variations in CYP19A1 were associated with hormone levels (estrone: Prs11070844 = 0.009, estrone sulphate: Prs11070844 = 0.01, Prs749292 = 0.004, Prs1062033 = 0.007 and Prs10519297 = 0.03, and sex hormone-binding globulin (SHBG): Prs3751591 = 0.03) and interacted with alcohol intake in relation to hormone levels (estrone sulphate: Pinteraction/rs2008691 = 0.02 and Pinteraction/rs1062033= 0.03, and SHBG: Pinteraction/rs11070844 = 0.03). CYP19A1/rs3751591 was both associated with SHBG levels (P = 0.03) and with risk of BC (Incidence Rate Ratio = 2.12; 95 % Confidence Interval: 1.02–4.43) such that homozygous variant allele carriers had increased levels of serum SHBG and were at increased risk of BC. Acute intake of alcohol decreased blood estrone (P = <0.0001), estrone sulphate (P = <0.0001), and SHBG (P = 0.009) levels, whereas Ibuprofen intake and PPARG Pro12Ala genotype had no effect on hormone levels.ConclusionsOur results suggest that genetically determined variation in CYP19A1 is associated with differences in sex hormone levels. However, the genetically determined differences in sex hormone levels were not convincingly associated with BC risk. The results therefore indicate that the genetically determined variation in CYP19A1 contributes little to BC risk and to alcohol-mediated BC risk.Trial registrationNCT02463383, June 3, 2015.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2317-y) contains supplementary material, which is available to authorized users.

The effect of acute ingestion of alcohol at 0.05% and 0.10% blood respiratory alcohol concentration on heterophoria

Introduction: Alcohol ingestion has a significant effect on speech, vision and coordination. The legal limit for driving under the influence in South Africa is 0.05% blood alcohol concentration (BAC), whilst intoxication is considered to occur at 0.10% BAC. The aim of our study was to investigate the effect of acute alcohol ingestion of 0.05% and 0.10% blood respiratory alcohol concentration (BrAC) on heterophoria.Methodology: The effect of alcohol ingestion on the oculomotor systems of 31 subjects was the basis of this quasi-experimental quantitative study. Various parameters were compared before and after the ingestion of 10% alc red wine. The Alcoscan ALP-1 breathalyser test was used as an indicator of BrAC. Heterophoric, fusional vergence and near point of convergence (NPC) measurements were measured during an experimental phase at 0.05% and 0.10% BrAC levels and a control phase at a 0% BrAC.Results: Mean changes in heterophoria for distance showed an increase of 1.13∆ ± 1.34∆ and 2.19∆ ± 1.70∆ towards esophoria at a BrAC of 0.05% and 0.10% respectively. At near, the results showed a mean increase of 0.84∆ ± 1.75∆ and 0.97∆ ± 1.70∆ towards exophoria at a BrAC of 0.05% and 0.10% respectively. There was a further mean decrease in the positive and negative fusional vergences as well as receded NPC break and recovery measurements at 0.05% and 0.10% BAC.Conclusion: It can be concluded that a BrAC of 0.05% has a minimal effect on heterophoria. However, at a BrAC of 0.1% there is a significant effect on heterophoria, fusional vergences and the NPC. This may or may not be clinically significant.

Exercise capacity is not impaired after acute alcohol ingestion: a pilot study.

The usage of alcohol is widespread, but the effects of acute alcohol ingestion on exercise performance and the stress hormone axis are not fully elucidated.We studied 10 healthy white men, nonhabitual drinkers, by Doppler echocardiography at rest, spirometry, and maximal cardiopulmonary exercise test (CPET) in two visits (2-4 days in between), one after administration of 1.5 g/kg ethanol (whisky) diluted at 15% in water, and the other after administration of an equivalent volume of water. Plasma levels of NT-pro-BNP, cortisol, and adrenocorticotropic hormone (ACTH) were also measured 10 min before the test, at maximal effort and at the third minute of recovery. Ethanol concentration was measured from resting blood samples by gas chromatography and it increased from 0.00 ± 0.00 to 1.25 ± 0.54‰ (P < 0.001). Basal echocardiographic and spirometric parameters were normal and remained so after acute alcohol intake, whereas ACTH, cortisol, and NT-pro-BNP nonsignificantly increased in all phases of the test. CPET data suggested a trend toward a slight reduction of exercise performance (peak VO2 = 3008 ± 638 vs. 2900 ± 543 ml/min, ns; peak workload = 269 ± 53 vs. 249 ± 40 W, ns; test duration 13.7 ± 2.2 vs. 13.3 ± 1.7 min, ns; VE/VCO2 22.1 ± 1.4 vs. 23.3 ± 2.9, ns). Ventilatory equivalent for carbon dioxide at rest was higher after alcohol intake (28 ± 2.5 vs. 30.4 ± 3.2, P = 0.039) and maximal respiratory exchange ratio was lower after alcohol intake (1.17 ± 0.02 vs. 1.14 ± 0.04, P = 0.04). In conclusion, we showed that acute alcohol intake in healthy white men is associated with a nonsignificant exercise performance reduction and stress hormone stimulation, with an unchanged exercise metabolism.

Effect of Acute Alcohol Ingestion on Resistance Exercise-Induced mTORC1 Signaling in Human Muscle.

Duplanty, AA, Budnar, RG, Luk, HY, Levitt, DE, Hill, DW, McFarlin, BK, Huggett, DB, and Vingren, JL. Effect of acute alcohol ingestion on resistance exercise-induced mTORC1 signaling in human muscle. J Strength Cond Res 31(1): 54-61, 2017-The purpose of this project was to further elucidate the effects postexercise alcohol ingestion. This project had many novel aspects including using a resistance exercise (RE) only exercise design and the inclusion of women. Ten resistance-trained males and 9 resistance-trained females completed 2 identical acute heavy RE trials (6 sets of Smith machine squats) followed by ingestion of either alcohol or placebo. All participants completed both conditions. Before exercise (PRE) and 3 (+3 hours) and 5 (+5 hours) hours postexercise, muscle tissue samples were obtained from the vastus lateralis by biopsies. Muscle samples were analyzed for phosphorylated mTOR, S6K1, and 4E-BP1. For men, there was a significant interaction effect for mTOR and S6K1 phosphorylation. At +3 hours, mTOR and S6K1 phosphorylation was higher for placebo than for alcohol. For women, there was a significant main effect for time. mTOR phosphorylation was higher at +3 hours than at PRE and at +5 hours. There were no significant effects found for 4E-BP1 phosphorylation in men or women. The major findings of this study was that although RE elicited similar mTORC1 signaling both in men and in women, alcohol ingestion seemed to only attenuate RE-induced phosphorylation of the mTORC1 signaling pathway in men. This study provides evidence that alcohol should not be ingested after RE as this ingestion could potentially hamper the desired muscular adaptations to RE by reducing anabolic signaling, at least in men.

Acute Behavioral and Long-Term Health Effects of Moderate Alcohol Use in Older Adults

This review addresses current literature regarding health consequences associated with of a lifestyle or pattern of moderate drinking and the neurobehavioral effects of moderate drinking episodes in older adults. Discussed studies include both large-scale epidemiological investigations of the effect of moderate alcohol use on multiple health-related domains (e.g., cancer and cardiovascular disease risk) in older adults and laboratory investigations of moderate alcohol’s acute neurobehavioral effects. Numerous studies provide evidence that a pattern of moderate drinking is associated with both potential health benefits and risks for older adults, including evidence for reduced risk of cardiovascular disease and cognitive decline but elevated risk for some cancers, including of the oral cavity, esophagus, and breast. Furthermore, laboratory administration studies indicate that older adults may be more susceptible to neurobehavioral alteration as a result of acute moderate alcohol intake than their younger counterparts. It is clear from the extant literature that even relatively low BACs resulting from the practice of a moderate drinking lifestyle are not without risk. This risk should be balanced against potential benefits at the level of the individual drinker. Additional studies regarding moderate drinking in older adults are needed to address limitations of the literature, including consideration of potential sex effects, inclusion of less rarified samples in acute studies, and the use of longitudinal, prospective designs.

Selective effects of acute alcohol intake on the prospective and retrospective components of a prospective-memory task with emotional targets.

Prospective memory involves remembering to do something in the future and has a prospective component (remembering that something must be done) and a retrospective component (remembering what must be done and when it must be done). Initial studies reported an impairment in prospective-memory performance due to acute alcohol consumption. Retrospective-memory studies demonstrated that alcohol effects vary depending on the emotionality of the information that needs to be learned. The aim of the present study was to investigate possible differential effects of a mild acute alcohol dose (0.4 g/kg) on the prospective and retrospective components of prospective memory depending on cue valence. Seventy-five participants were allocated to an alcohol or placebo group and performed a prospective-memory task in which prospective-memory cue valence was manipulated (negative, neutral, positive). The multinomial model of event-based prospective memory (Smith and Bayen 2004) was used to measure alcohol and valence effects on the two prospective-memory components separately. Overall, no main effect of alcohol or valence on prospective-memory performance occurred. However, model-based analyses demonstrated a significantly higher retrospective component for positive compared with negative cues in the placebo group. In the alcohol group, the prospective component was weaker for negative than for neutral cues and the retrospective component was stronger for positive than for neutral cues. Group comparisons showed that the alcohol group had a significantly lower prospective component for negative cues and a lower retrospective component for neutral cues. This is the first study to demonstrate selective alcohol effects on prospective-memory components depending on prospective-memory cue valence.

Binge-like ingestion of a combination of an energy drink and alcohol leads to cognitive deficits and motivational changes

The combination of alcohol with an energy drink (ED) is believed to contribute to risky alcohol-drinking behaviors, such as binge drinking. However, the long-term effects on cognition and reward function that are caused by the repeated binge-like ingestion of alcohol and EDs are still poorly known. The present study examined the effects of a history of repeated exposure to alcohol and/or an ED on short-term memory and alcohol-seeking behavior. Male Wistar rats were given daily intragastric administration of alcohol (3.4g/kg) combined or not with an ED (10.71ml/kg) for 6 consecutive days. The rats were tested for locomotion 15min after the first intragastric treatment. Short-term memory was assessed in the novel object recognition and social discrimination tests 2–3days after the last intragastric administration. The rewarding effect of alcohol was tested 1–3weeks following the last intragastric administration in a conditioned place preference paradigm. The acute binge-like ingestion of alcohol decreased locomotor activity, whereas the combination of alcohol and an ED increased locomotion in the first minutes of assessment. Alcohol exposure produced cognitive deficits in both the object recognition and social discrimination tests, and adding the ED to the alcohol solution did not modify these effects. The combination of alcohol and the ED increased alcohol-induced conditioned place preference. Thus, a history of binge-like alcohol exposure combined with the ED caused subsequent cognitive deficits and increased alcohol seeking behavior, and such behavioral effects might contribute to the progression to alcohol abuse disorders.

Effect of GABA Extract of Black Sticky Rice with Giant Embryo on Alcohol-Related Indices After Acute Alcohol Intake in Social Drinkers.

This study was performed to evaluate the effect and safety of a high-gamma-aminobutyric acid-containing extract (GABA extract) of black sticky rice with giant embryo (BSRGE) on alcohol-related indices after acute alcohol intake in social drinkers. Subjects were randomized to the GABA extract (G) group, GABA extract and alcohol drinking (GA) group, or placebo intake and alcohol drinking (PA) group in a double-blind design. All subjects were administered GABA extract (200mg GABA) or placebo at 9 am on study days 2 and 3, respectively. Subjects in the GA and PA groups were administered an equivalent dose of alcohol that was diluted in a drinking beverage for a total amount of 240ml at 11 am on day 3. Blood alcohol concentration (BAC) and the Biphasic Alcohol Effects Scale were measured just before alcohol drinking, and 6 times after alcohol drinking. The peak and area under the curve (AUC) of the total stimulation scale score after alcohol intake in females were significantly higher in the GA than in the PA group, whereas no significant difference was found between the 2 groups in males. The peak and AUC of the total score on the sedation scale after alcohol intake in males were significantly lower in the GA than in the PA group, whereas both were significantly higher in the GA than in the PA group of females. The AUC for BAC in males was significantly lower in the GA than in the PA group, whereas no significant difference was found in females. No adverse events were reported in any of the groups including the G group. Coadministration of a GABA extract to social drinkers while drinking alcohol is supposed to affect alcohol-related indices in terms of pharmacodynamics and pharmacokinetics and did not induce any adverse events.

Beer Is Less Harmful for the Liver than Plain Ethanol: Studies in Male Mice Using a Binge-Drinking Model.

Mechanisms involved in the less damaging effects of beer in comparison to hard spirits have not yet been fully understood. The aim of the study was to determine if the effect of beer intake on the liver differs from that of plain ethanol and if so to determine mechanisms involved. Male C57BL/6J mice received either ethanol, beer (ethanol content: 6 g/kg body weight) or iso-caloric maltodextrin solution. Markers of steatosis, lipogenesis, activation of the toll-like receptor-4 signaling cascade and lipid export in liver and tight junction proteins in duodenum were measured 6 and 12 h after acute ethanol or beer intake. Alcohol ingestion resulted in a significant increase of hepatic triglyceride accumulation 6 and 12 h after ingestion, respectively, being markedly lower in mice fed beer. Expression of sterol regulatory element-binding protein-1c mRNA was significantly lower 12 h after alcohol or beer exposure, while fatty acid synthase mRNA expression was induced in livers of ethanol-fed mice and to a lesser extent in mice fed beer 6 h after acute alcohol ingestion. Protein levels of tight junction proteins in the small intestine were similar between groups while expression of myeloid differentiation primary response gene 88 in livers was significantly induced in ethanol- but not in beer-fed mice. Concentrations of 4-hydroxynonenal protein adducts and inducible nitric oxide synthase protein were also only induced in livers of mice fed ethanol. Protein levels of apolipoprotein B were induced in livers of beer-fed mice only. Our data suggest that beer is less harmful on the development of acute alcohol-induced liver damage than plain ethanol in male mice.

Acute oral ingestion of alcohol modulates muscle sympathetic neural activity differently in Caucasians and African Americans

Recent studies consistently report that acute alcohol consumption increases muscle sympathetic nerve activity (MSNA) in humans. Despite the increased prevalence of hypertension and alcohol consumption in African Americans (AA), no studies have compared MSNA responses to alcohol consumption in AA and Caucasians (C). We hypothesized that alcohol consumption would increase MSNA in both AA and C, but that sympathoexcitatory responses would be augmented in AA. Five minutes of supine heart rate (HR), blood pressure, MSNA, and forearm blood flow were recorded in 8 AA (age, 23±1 yr) and 8 C (age, 22±1 yr) before and 45 min after consumption of 2.5ml of vodka per kg body mass. Increases in blood alcohol content (BAC) were greater in AA (0.105%) compared to C (0.087%; P&lt;0.05). Alcohol elicited similar increases of HR in AA (62±5 to 70±4 beats/min; p&lt;0.001) and C (62±5 to 68±5 beats/min; p&lt;0.001). Contrary to our initial hypothesis, alcohol consumption increased MSNA in C (14±3 to 27±5 bursts/100 heart beats; P&lt;0.05), but did not alter MSNA in AA (28±7 to 29±6 bursts/100 heart beats). Forearm vascular conductance (FVC) was not altered by alcohol consumption in AA or C. However, when sympathetic vascular transduction was calculated (i.e., FVC/MSNA), alcohol consumption reduced sympathetic vascular transduction in C (2.4±0.4 to 1.1±0.2 units; p&lt;0.01), but not AA (1.3±0.4 to 1.3±0.4 units). These findings suggest acute alcohol consumption influences resting MSNA and MSNA‐vascular coupling differently in AA and C, but it is unclear if the different levels of BAC, and perhaps rates of alcohol metabolism, are contributing to these racial differences.

Alcohol Use Disorders: Implications for the Clinical Toxicologist

Alcohol use disorders (AUDs) are a health problem of high prevalence in most communities and such problems account for 5% of the total burden of disease worldwide. Clinical toxicologists are commonly required to treat patients having AUDs and associated drug/alcohol-related harm. There have been recent changes to some of the diagnostic criteria (notably in DSM V) relevant to AUDs, with older terms “alcohol abuse” and “alcohol dependence” no longer being classified. AUDs may sometimes not be clearly recognizable and use of evidence-based screening interventions can help identify such conditions and lead to effective brief interventions (e.g. SBIRT programs in emergency departments). AUDs are viewed as chronic disorders of alcohol consumption occurring across a spectrum of severity. While most AUDs are mild to moderate in severity and usually self-limiting conditions, more severe presentations are more commonly encountered by physicians in emergency settings. Hence, clinical toxicologists are more likely to see patients within the more severe form of disorder, at end of the spectrum of AUDs. Among this group of patients, multi-morbidity and particularly high mortality risk exists, and thus they usually require management collaboration with specialist services. Patients with AUDs are most likely to be recognized by a clinical toxicologist in the following scenarios: following acute heavy alcohol ingestion and subsequently developing acute alcohol intoxication (ethanol toxidrome), following accidental or intentional drug overdosage where alcohol has also been consumed, following acute alcohol consumption that has been associated with behavioral risk-taking and/or self-harming (e.g. poisoning, envenomation, etc.), when alcohol withdrawal reactions are severe requiring hospitalization and possibly following an adverse drug reaction.

Dissolution of lipids from mucus: A possible mechanism for prompt disruption of gut barrier function by alcohol

Acute and/or chronic alcohol ingestion has been shown to exacerbate the morbidity and mortality rate associated with acute mechanical and/or thermal trauma. While alcohol ingestion can affect many organs and systems, clinical and preclinical studies indicate that alcohol ingestion can cause a ‘leaky gut’ syndrome which in turn contributes to infection and systemic organ dysfunction. This study investigated the acute effect of alcohol on gut barrier function. Using an in vivo isolated gut sac model of naïve male rats, each individual gut sac was injected with different concentrations (0, 5, 10, 20, and 40%, v/v) of alcohol. After different times of alcohol exposure, each isolated gut segment was harvested and intestinal permeability and mucosal surface hydrophobicity (a physiologic marker of mucus barrier function) were measured as well as luminal DNA, mucus, protein and free fatty acids. The results showed that alcohol caused dose-dependent and time-dependent increases in gut permeability and decreases in mucosal surface hydrophobicity, with significant changes to be observed 5min after treatment with 10% alcohol. In addition, it is further found that these changes in permeability and hydrophobicity are more closely associated with increased intestinal luminal free fatty acids levels but not protein or DNA levels. These results suggest that alcohol may cause loss of gut barrier function by extracting and dissolving lipids from the mucus with a resultant decrease in mucosal surface hydrophobicity, which is a critical component of gut barrier function.

Prospective study of alcohol consumption and self-reported hearing loss in women

Chronic excess alcohol intake has been associated with irreversible hearing loss and acute alcohol intake may temporarily impair auditory function; however, some evidence suggests that long-term moderate alcohol intake may be related to lower risk of hearing loss. This study prospectively examined the association between total alcohol and individual alcoholic beverage consumption and risk of hearing loss in women. Data were prospectively collected from 65,424 participants in the Nurses' Health Study II (NHS II), aged 27–44 years at baseline (follow-up 1991–2009). Alcohol consumption was assessed using a validated questionnaire every 4 years. An incident case was defined as a self-reported hearing problem that began after 1991. Cox proportional hazards multivariate regression was used to adjust for potential confounders. During 1,024,555 person-years of follow-up, 12,384 cases of hearing loss occurred. After multivariate adjustment, there was no significant association between total alcohol consumption and risk of hearing loss. In exploratory analyses, beer consumption was associated with increased risk and wine consumption was associated with reduced risk. No significant association was observed for consumption of liquor. Total alcohol consumption is not associated with risk of hearing loss in women. The modest associations observed for beer (direct) and wine (inverse) may be due to chance or residual confounding but merit further study.

Comparing the effects of acute alcohol consumption in germ-free and conventional mice: the role of the gut microbiota.

BackgroundIncreasing evidence suggest that the gut microbiota plays an important role in liver pathology after acute alcohol intake. The aim of our study was to investigate the roles played by commensal bacteria in alcohol-induced liver injury and in the dysbiosis caused by alcohol intake in germ-free mice, as well as the possibility of protection against alcohol-induced injuries in animals fed a high-fiber diet. For these purposes, germ-free and conventional mice were submitted to acute alcohol intake, consisting of administration of ethanol in their drinking water for 7 days, with a higher dose of alcohol administered on day 7.ResultsThere was no liver injury after alcohol consumption, and there was less neutrophil infiltration and lower pro-inflammatory cytokine levels (CXCL-1/KC and interleukin (IL)-6) in the liver in germ-free mice compared with alcohol-fed conventional mice. Additionally, conventionalization of germ-free mice with intestinal contents from alcohol-fed conventional mice induced injury and inflammation in both the liver and the intestine, suggesting that alcohol intake successively caused a perturbation of the intestinal microbiota (dysbiosis) and liver injury. Finally, previous treatment with a high-fiber diet decreased liver injury and gut permeability in alcohol-fed conventional mice.ConclusionsIn conclusion, the results of the present study provide evidence that the gut microbiota plays an important role in alcohol-induced liver injury, apparently through dysbiosis of the intestinal microbial ecosystem caused by alcohol intake. Furthermore, treatment with a high-fiber diet can counteract hepatocyte pathology and gut leakage and thus could be a promising therapeutic option.Electronic supplementary materialThe online version of this article (doi:10.1186/s12866-014-0240-4) contains supplementary material, which is available to authorized users.

Treatment refractory mood disorders: Case report

CASE BF is a 42 year-old Caucasian male who reported his onset of depression began four years ago after he was involved in a car accident that fractured his hip. He was not treated for depression until he overdosed on approximately 50 aspirin 325 mg tablets and 750 ml of whiskey (seven months following the accident). After being medically cleared from the emergency room and acute inpatient unit, he was transferred to inpatient psychiatry for evaluation of depression. Upon admission to the inpatient psychiatric unit, his labs were found to be within normal limits (WNL) except a slight elevation in gamma-glutamyl transferace (GGT) at 51 U/L, likely from his acute alcohol ingestion. His thyroid panel was also WNL. He denied any other illness or taking any other medications.