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Heavy Alcohol Consumption (heavy + alcohol_consumption)

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Medical Sciences	100%

Selected Abstracts

The Effect of Moderate to Heavy Alcohol Consumption on Neuropsychological Performance as Measured by the Repeatable Battery for the Assessment of Neuropsychological Status

ALCOHOLISM, Issue 3 2010
Alisa Green
Background:, Excessive alcohol use is associated with damage to the structure and function of the brain and impairment of cognition and behavior. Traditional test batteries used to assess cognitive performance in alcoholics are extensive and costly, limiting their use across various clinical and research settings. The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) is a relatively new instrument that attempts to overcome some of these limitations. As yet the individual effect of moderate to heavy alcohol consumption on RBANS performance has not been examined. The primary aim of this study was to explore and quantify differences in performance between controls and drinkers on the RBANS and to examine the influence of age, gender, and alcohol use patterns on test performance. Methods:, Data from a subset of "Using Our Brains" (UoB) donors (n = 28) still actively drinking and meeting criteria for moderate to heavy alcohol use (30 to 80 g of ethanol per day) (Harper, 1988) and 28 matched controls (age, education, and premorbid Intelligence Quotient) were compared. Results:, Participants in the alcohol group performed below the healthy control group on the visuospatial and immediate memory index, and also on the RBANS total score p < 0.001 and showed a greater decline in RBANS scores from estimated cross-sectional premorbid levels. There was a positive association between alcohol ingestion in the preceding 12 months and the language index p < 0.03 and the semantic fluency subtest (p < 0.03). Age was negatively associated with story memory (p < 0.02), coding (p < 0.001), list recognition (p < 0.01), story recall (p < 0.03), and figure recall (p < 0.02). Conclusion:, Our results suggest that the RBANS is able to detect and characterize differences in verbal fluency, visuospatial skills, components of declarative memory, and psychomotor speed between healthy controls and moderate to heavy active alcohol users. Executive functions, commonly affected by alcoholism and not included in the RBANS, require assessment with additional measures. [source]

Alcohol Up-Regulates TLR2 Through a NO/cGMP Dependent Pathway

ALCOHOLISM, Issue 1 2010
Kristina L Bailey
Background:, Heavy alcohol consumption is associated with severe bronchitis. This is likely related to increased inflammation in the airways of alcohol abusers. Toll-like receptor 2 (TLR2) is an important mediator of inflammation in the airway epithelium. TLR2 initiates an inflammatory cascade in response to gram-positive bacteria. We have previously shown that alcohol up-regulates TLR2 in the airway epithelium. However, the mechanism of alcohol-mediated up-regulation of TLR2 has not been identified. Methods:, A human airway epithelial cell line, 16HBE14o,, was exposed to biologically relevant concentrations of alcohol (100 mM) in the presence and absence of N, -Nitro- l -arginine methyl ester hydrochloride, a nitric oxide (NO) synthase inhibitor; and Rp-8-Br-cGMP-S, an antagonist analogue of cGMP. TLR2 was measured using real-time PCR and Western blots. In addition, 16HBE14o, cells were incubated with sodium nitroprusside (SNP), an NO donor, and 8-Br-cGMP, a cGMP analogue. TLR2 was measured using real-time PCR. Results:,N, -Nitro- l -arginine methyl ester hydrochloride blocked the alcohol-mediated up-regulation of TLR2. This indicates that NO plays a key role in alcohol's up-regulation of TLR2. SNP, a NO donor, up-regulated TLR2. Rp-8-Br-CGMP-S attenuated alcohol's up-regulation of TLR2, suggesting that NO was working through cGMP/PKG. 8-Br-cGMP up-regulated TLR2, also demonstrating the importance of cGMP/PKG. Conclusions:, Alcohol up-regulates TLR2 through a NO/cGMP/PKG dependent pathway in the airway epithelium. This is an important observation in the understanding how alcohol modulates airway inflammation. In addition, this is the first time that cyclic nucleotides have been shown to play a role in the regulation of TLR2. [source]

Ethanol Promotes Thiamine Deficiency-Induced Neuronal Death: Involvement of Double-Stranded RNA-activated Protein Kinase

ALCOHOLISM, Issue 6 2009
Zun-Ji Ke
Background:, Heavy alcohol consumption causes cerebellar degeneration, and the underlying mechanism is unclear. Chronic alcoholism is usually associated with thiamine deficiency (TD) which is known to induce selective neurodegeneration in the brain. However, the role of TD in alcohol-induced cerebellar degeneration remains to be elucidated. The double-stranded RNA-activated protein kinase (PKR) is a potent antiviral protein. Viral infection or binding to dsRNA causes PKR autophosphorylation and subsequent phosphorylation of the ,-subunit of eukaryotic translation factor-2,, leading to inhibition of translation or apoptosis. PKR can also be activated by cellular stresses. Methods:, In this study, we used an in vitro model, cultured cerebellar granule neurons (CGNs), to investigate the interaction between TD and ethanol and evaluate the contribution of their interaction to neuronal loss. TD was induced by treatment with amprolium in association with ethanol. Cell viability was determined by 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide assay. PKR expression/phosphorylation and subcellular distribution was analyzed with immunoblotting and immunocytochemistry. Results:, Thiamine deficiency caused death of CGNs but ethanol did not. However, TD plus ethanol induced a much greater cell loss than TD alone. TD-induced PKR phosphorylation and ethanol exposure significantly promoted TD-induced PKR phosphorylation as well as its nuclear translocation. A selective PKR inhibitor not only protected CGNs against TD toxicity, but also abolished ethanol potentiation of TD-induced loss of CGNs. Conclusions:, Ethanol promoted TD-induced PKR activation and neuronal death. PKR may be a convergent protein that mediates the interaction between TD and ethanol. [source]

BRIEF EXPOSURE TO ETHANOL AUGMENTS VASCULAR CONTRACTILITY IN HUMAN CHORIONIC PLATE ARTERIES

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2004
Eun Hui Hong
Summary 1.,Heavy alcohol consumption has been known as a risk factor for hypertension, although the mechanism by which alcohol intake causes hypertension remains elusive. 2.,We tested the hypothesis that brief exposure to ethanol augments vascular contractility through the stress response in human chorionic plate arteries. 3.,Human chorionic plate arteries were mounted in organ baths and exposed to 5% ethanol for 15, 30 or 45 min. 4.,Brief exposure for 45 min, but not 15 min, not only augmented contractility to KCl and 5-hydroxytryptamine 5 h after the end of exposure, but also increased the expression of heat shock protein (HSP) 70 in the tissues. 5.,Reverse transcription,polymerase chain reaction showed gradual increases of hsp70 mRNA expression, but not heat shock cognate 70 (hsc70), hsp90, or glucose regulatory protein 78 (grp78) mRNA expression, in an exposure time-dependent manner 3 h after the end of exposure. 6.,These results indicate that ethanol augments vascular contractility through the stress response. [source]

Social consumption of alcohol in adolescents with Type 1 diabetes is associated with increased glucose lability, but not hypoglycaemia

DIABETIC MEDICINE, Issue 8 2006
D. Ismail
Abstract Aims To determine the effects of social consumption of alcohol by diabetic adolescents on glycaemic control. Methods Fourteen (five male) patients aged > 16 years were recruited from the diabetes clinic at the Royal Children's Hospital. The continuous glucose monitoring system (CGMS) was attached at a weekend when alcohol consumption was planned for one night only. For each patient, the 12-h period from 18.00 h to 06.00 h for the night with alcohol consumption (study period) was compared with the same period with non-alcohol consumption (control period) either 24 h before or after the alcohol study night. Thus, each subject was his/her own control. Glycaemic outcomes calculated from continuous glucose monitoring included mean blood glucose (MBG), percentage of time spent at low glucose levels (CGMS < 4.0 mmol/l), normal glucose levels (CGMS 4.0,10.0 mmol/l) and high glucose levels (> 10.0 mmol/l) and continuous overall net glycaemic action (CONGA). Results The mean number of standard alcohol drinks consumed during the study period was 9.0 for males and 6.3 for females. There was no difference in percentage of time at high and normal glucose levels in the study and control periods. During the control period, there was a higher percentage of time with low glucose levels compared with the study period (P < 0.05). There was an increased level of glycaemic variation during the study time when compared with the control period. Conclusions In an uncontrolled, social context, moderately heavy alcohol consumption by adolescents with Type 1 diabetes appears to be associated with increased glycaemic variation, but not with low glucose levels. [source]

Correlation between heavy alcohol consumption and elevation of matrix metalloproteinases

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 4 2002
R. Forough
No abstract is available for this article. [source]

Exploring the link between microorganisms and oral cancer: A systematic review of the literature

HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 9 2009
Samuel J. Hooper PhD
Abstract The majority of cases of oral cancer have been related to tobacco use and heavy alcohol consumption. However, the incidence of oral cavity carcinoma appears to be increasing in many parts of the world in a manner that it is difficult to explain with traditional risk factors alone. Meanwhile, interest in the possible relationships between microorganisms and the different stages of cancer development has been rising and numerous mechanisms by which bacteria and yeast may initiate or promote carcinogenesis are currently under investigation. In particular, a persuasive body of evidence suggests a possible etiological role involving the metabolism and production of carcinogenic products, such as acetaldehyde. Other suggested mechanisms include the induction of chronic inflammation and direct interference with eukaryotic cell cycle and signaling pathways. This review aims to summarize the known associations between microbial infection and cancer and draw attention to how they may relate to oral carcinoma. © 2009 Wiley Periodicals, Inc. Head Neck, 2009 [source]

Experimental acute alcohol pancreatitis-related liver damage and endotoxemia: synbiotics but not metronidazole have a protective effect

JOURNAL OF DIGESTIVE DISEASES, Issue 4 2005
F MAROTTA
OBJECTIVE: The aim of this study was to test the effect of gut manipulation by either novel synbiotics or by metronidazole on either endotoxemia or the severity of liver damage in the course of acute pancreatitis from alcohol ingestion. METHODS: Sprague,Dawley rats were fed for 1 week through an intragastric tube a liquid diet with either: (i) 1 mL t.i.d. of a mixture of synbiotics (Lactobacillus acidophilus, Lactobacillus helveticus and Bifidobacterium in an enriched medium); (ii) 20 mg/kg t.i.d. metronidazole; or (iii) standard diet. Then, acute pancreatitis was induced by caerulein and when the disease was full-blown, rats were fed an alcohol-rich diet. Synbiotic and metronidazole treatment was given for a further 2 weeks. Transaminase and endotoxemia levels were measured before treatment, after 6 h, after 24 h and 2 weeks later, at the time the rats were killed. Liver samples were obtained for histological analysis. RESULTS: Synbiotics but not metronidazole improved the acute pancreatitis-induced increase in endotoxemia and transaminase levels. The addition of alcohol worsened these variables to a limited extent in the synbiotic-treated group, while metronidazole had a negative effect on liver damage. CONCLUSIONS: Gut flora pretreatment with synbiotics was able to effectively protect against endotoxin/bacterial translocation, as well as liver damage in the course of acute pancreatitis and concomitant heavy alcohol consumption. The beneficial effect of synbiotics on liver histology seems to be correlated with endotoxemia. Metronidazole did not produce such a beneficial effect; in fact, it further worsened liver damage when alcohol was added to the background of ongoing acute pancreatic inflammation. [source]

The Effect of Moderate to Heavy Alcohol Consumption on Neuropsychological Performance as Measured by the Repeatable Battery for the Assessment of Neuropsychological Status

Phosphatidylethanol and Alcohol Consumption in Reproductive Age Women

ALCOHOLISM, Issue 3 2010
Scott H. Stewart
Background:, Fetal alcohol disorders are preventable, but self-reported alcohol consumption can be misleading and impede effective treatment. Biomarkers represent an alternative method for assessing alcohol use, and this study evaluated the relationship between blood phosphatidylethanol (PEth) and alcohol use in a sample of reproductive age women. Methods:, Alcohol use was estimated by validated self-report methods in 80 nonpregnant women ages 18 to 35. PEth was measured by a contracted laboratory using a liquid chromatography-tandem mass spectrometry assay. Regression methods appropriate for the distribution of PEth were used to define its relationship to alcohol consumption during the prior 2 weeks and explore the effects of drinking patterns on this association. Receiver operating characteristic analysis was used to estimate the sensitivity of PEth for various drinking levels at 95% specific cutoffs. Results:, PEth had a positive linear association with grams of alcohol consumed (p < 0.001), and was detectable in 93% of subjects consuming an average of 2 or more drinks per day. The relationship between total alcohol consumption and PEth may be stronger in women with recent heavy drinking days. The relationship between drinking and PEth varied considerably between individuals, and sensitivity for a certain amount of drinking was low at a highly specific cutoff concentration. Conclusions:, PEth is a highly sensitive indicator of moderate and heavy alcohol consumption in reproductive age women and may complement the use of self-report alcohol screens when additional objective markers of alcohol use are desirable. However, choosing a highly valid cutoff concentration for PEth to differentiate various levels of alcohol consumption may not be feasible. [source]

Blood Glucose Level, Alcohol Heavy Drinking, and Alcohol Craving During Treatment for Alcohol Dependence: Results From the Combined Pharmacotherapies and Behavioral Interventions for Alcohol Dependence (COMBINE) Study

ALCOHOLISM, Issue 9 2009
Lorenzo Leggio
Background:, Heavy drinking may increase blood glucose levels. Moreover, in alcohol-dependent subjects, glucose may play a putative role in alcohol preference. Methods:, This study investigated the relationship between blood glucose levels and both alcohol heavy drinking and craving in alcohol-dependent subjects participating in the COMBINE Study. The primary objective was to evaluate the relationship between baseline (pretreatment) glucose levels and percentage of heavy drinking day (PHDD) during treatment. The secondary objective was to evaluate the relationship between glucose levels, baseline PHDD, and craving measured by the Obsessive Compulsive Drinking Scale (OCDS). Results:, This analysis consisted of 1,324 participants. Baseline glucose levels were significantly and positively associated with PHDD during treatment [F(1, 1225) = 5.21, p = 0.023], after controlling for baseline PHDD [F(1, 1225) = 36.25, p < 0.0001], gender [F (1, 1225) = 3.33, p = 0.07], and body mass index (BMI) [F(1, 1225) = 0.31, p = 0.58]. Higher glucose levels at baseline were associated with a higher percentage of PHDD at pretreatment [F(1, 1304) = 5.96, p = 0.015], after controlling for gender [F(1, 1304) = 0.29, p = 0.59] and BMI [F(1, 1304) = 0.90, p = 0.34]. Glucose was not significantly associated with the OCDS total score [F(1, 1304) = 0.12, p = 0.73], the OCDS Obsessive subscale [F(1, 1304) = 0.35, p = 0.56], or the OCDS Compulsive subscale [F(1, 1304) = 1.19, p = 0.28] scores, after controlling for gender and BMI. Discussion:, A link between pretreatment glucose levels and heavy drinking during treatment was found, suggesting a role of glucose in predicting heavy alcohol consumption. Although caution is needed in the interpretation of these results, elevated glucose and heavy drinking may be affected by a common mechanism and manipulations affecting glucose regulation may influence alcohol consumption. [source]

Alcohol Consumption, Social Support, and Risk of Stroke and Coronary Heart Disease Among Japanese Men: The JPHC Study

ALCOHOLISM, Issue 6 2009
Satoyo Ikehara
Background:, It is unclear whether the association between alcohol consumption and risk of cardiovascular disease is affected by social support. Methods:, The prospective data for 19,356 men aged 40 to 69 years who participated in the Japan Public Health Center-Based Prospective Study. Alcohol consumption was classified into 7 categories: never, past, occasional, 1 to 149, 150 to 299, 300 to 449, or ,450 g ethanol/wk. Associations between alcohol consumption and risk of cardiovascular disease were stratified by the median level of social support score, which was measured in emotional support score of this cohort study. Results:, During an average follow-up of 9.9 years, 629 total strokes and 207 coronary heart diseases were documented. Light-to-moderate alcohol consumption was associated with reduced risks of coronary heart disease and total cardiovascular disease, while heavy alcohol consumption was associated with increased risk of total stroke, in particular hemorrhagic stroke. When stratified by social support score, the multivariable hazard ratios of total cardiovascular disease associated with light-to-moderate alcohol consumption (1 to 299 g/wk) were 0.99 (0.72 to 1.37) in the low social support group and 0.56 (0.44 to 0.70) in the high social support group (p for interaction = 0.002), while the multivariable hazard ratios of hemorrhagic stroke associated with heavy alcohol consumption (,300 g/wk) were 2.09 (1.03 to 4.27) in the low social support group and 1.25 (0.72 to 2.15) in the high social support group (p for interaction = 0.44). There was no interaction between alcohol consumption and social support in relation to risk of coronary heart disease. Conclusions:, Social support may enhance the beneficial effect of light-to-moderate alcohol consumption on risk of cardiovascular disease. [source]

Disparities in Alcohol-Related Problems Among White, Black, and Hispanic Americans

ALCOHOLISM, Issue 4 2009
Nina Mulia
Background:, This study assesses racial/ethnic disparities in negative social consequences of drinking and alcohol dependence symptoms among white, black, and Hispanic Americans. We examine whether and how disparities relate to heavy alcohol consumption and pattern, and the extent to which social disadvantage (poverty, unfair treatment, and racial/ethnic stigma) accounts for observed disparities. Methods:, We analyzed data from the 2005 U.S. National Alcohol Survey, a nationally representative telephone-based survey of adults ages 18 and older (N = 6,919). Given large racial/ethnic differences in abstinence rates, core analyses were restricted to current drinkers (N = 4,080). Logistic regression was used to assess disparities in alcohol-related problems at 3 levels of heavy drinking, measured using a composite variable incorporating frequency of heavy episodic drinking, frequency of drunkenness, and maximum amount consumed in a single day. A mediational approach was used to assess the role of social disadvantage. Results:, African American and Hispanic drinkers were significantly more likely than white drinkers to report social consequences of drinking and alcohol dependence symptoms. Even after adjusting for differences in heavy drinking and demographic characteristics, disparities in problems remained. The racial/ethnic gap in alcohol problems was greatest among those reporting little or no heavy drinking, and gradually diminished to nonsignificance at the highest level of heavy drinking. Social disadvantage, particularly in the form of racial/ethnic stigma, appeared to contribute to racial/ethnic differences in problems. Conclusions:, These findings suggest that to eliminate racial/ethnic disparities in alcohol-related problems, public health efforts must do more than reduce heavy drinking. Future research should address the possibility of drink size underestimation, identify the particular types of problems that disproportionately affect racial/ethnic minorities, and investigate social and cultural determinants of such problems. [source]

HDL2 of Heavy Alcohol Drinkers Enhances Cholesterol Efflux From Raw Macrophages via Phospholipid-Rich HDL2b Particles

ALCOHOLISM, Issue 6 2008
Sanna M. Mäkelä
Background:, Alcohol consumption is associated with increased serum high density lipoprotein (HDL) cholesterol levels and a decreased risk for the development of atherosclerosis. However, the effects of heavy alcohol intake on reverse cholesterol transport, one of the key anti-atherogenic processes related to HDL, are poorly known. Methods:, The ability of total HDL as well as HDL2 and HDL3 subclasses to promote cholesterol efflux from 3H-cholesterol-labeled RAW 264.7 macrophages was studied among 6 heavy alcohol drinkers and 6 controls. Distribution of HDL subclasses was analyzed by 4 to 30% native gradient gels. Serum phospholipid transfer protein (PLTP) and cholesteryl ester transfer protein (CETP) activities were analyzed among several other biochemical measures. Results:, Cholesterol efflux to HDL2 of heavy drinkers was 22% (p = 0.025) higher relative to controls. The increase in HDL2 phospholipids, with a concomitant 2-fold (p = 0.055) increase in large HDL2b particles, was associated with enhanced cholesterol efflux to HDL2. Interestingly, the cholesterol efflux to HDL3 did not differ between the 2 study groups. These findings may be partially explained by a decreased CETP activity (,26%, p = 0.037) and an increased PLTP activity (39%, p = 0.045) in heavy drinkers. Conclusions:, The increased cholesterol efflux potential of HDL2 is most likely an anti-atherogenic feature linked to heavy alcohol consumption. The cholesterol efflux and HDL phospholipids also associated strongly within the whole study group (rs = 0.910, p , 0.01) suggesting a common pathway of enhanced cholesterol efflux via enlarged phospholipid-rich HDL particles. [source]

Ethanol Modulation of TNF-alpha Biosynthesis and Signaling in Endothelial Cells: Synergistic Augmentation of TNF-alpha Mediated Endothelial Cell Dysfunctions by Chronic Ethanol

ALCOHOLISM, Issue 6 2005
Corinne Luedemann
Despite reported cardio-protective effects of low alcohol intake, chronic alcoholism remains a risk factor in the pathogenesis of coronary artery disease. Dose related bimodal effects of alcohol on cardiovascular system might reflect contrasting influences of light versus heavy alcohol consumption on the vascular endothelium. Chronic ethanol induced damage to various organs has been linked to the increased release of TNF-alpha (TNF). We have previously shown that TNF, expressed at the sites of arterial injury, suppresses re-endothelialization of denuded arteries and inhibits endothelial cell (EC) proliferation in vitro. Here we report that in vitro chronic ethanol exposure enhances agonist-induced TNF mRNA and protein expression in EC. Ethanol-mediated increment in TNF expression involves increased de novo transcription without affecting mRNA stability. DNA binding assays revealed that ethanol-induced TNF up regulation was AP1 dependent. Functionally, TNF induced EC dysfunction, including reduced proliferation, migration and cyclin A expression, were all markedly enhanced in the presence of ethanol. Additionally, expression of cyclin D1 was significantly attenuated in cells co-treated with TNF and ethanol while each treatment alone had little effect on cyclin D1 expression. Furthermore, exposure to ethanol potentiated and prolonged agonist-induced activation of JNK. Inhibition of JNK by over-expression of dominant negative JNK1 substantially reversed ethanol/TNF-mediated inhibition of cyclin A expression and EC proliferation, suggesting modulation of JNK1 signaling as the mechanism for ethanol/TNF-induced EC dysfunctions. Taken together, these data indicate that chronic ethanol consumption may negatively influence post angioplasty re-endothelialization thereby contributing to the development of restenosis. [source]

Biological Markers of Alcohol Consumption in Nondrinkers, Drinkers, and Alcohol-Dependent Brazilian Patients

ALCOHOLISM, Issue 7 2002
N. B. Figlie
Background The purpose of this study was to compare the sensitivity and specificity of some new and traditional biological markers and indicators of health among Brazilian nondrinkers, drinkers, and alcohol-dependent patients. Material and Methods We evaluated 130 nondrinkers, 167 drinkers, and 183 alcohol-dependent drinkers from Brazil who participated in the WHO/ISBRA Study on State and Trait Markers of Alcohol Use and Dependence. A standardized WHO/ISBRA Interview Schedule provided background information on the subjects' characteristics including reported health problems and alcohol consumption. Blood samples were analyzed for aspartate aminotransferase (AST), carbohydrate deficient transferrin (CDT), ,-glutamyltransferase (GGT), blood alcohol levels (BAL), and platelet adenylate cyclase activity (basal levels [AC] and levels after stimulation with Gpp(NH)p, cesium fluoride, and forskolin). Results The alcohol-dependent drinkers presented higher levels of AST, GGT, AC, CDT, and BAL than the nondrinkers and drinkers, whose levels were similar. Sex differences in the sensitivity of CDT and AC were found. The alcohol-dependent women presented a lower prevalence of abnormal values of CDT and Gpp(NH)p-stimulated AC than the alcohol-dependent men, despite the fact that they presented similar alcohol consumption levels. The alcohol-dependent drinkers presented a higher prevalence of clinical disorders than the nondrinkers and drinkers. The drinkers and alcohol-dependent patients presented significantly higher rates of gastritis than the nondrinkers. Conclusions Sex differences in the sensitivity of CDT and AC suggest that these markers are not as sensitive at detecting excessive alcohol use in women as they are in men. If data from this Brazilian sample are compared with those reported for international samples, relevant differences are detected, which suggests that genetic and cultural differences should be considered in the selection of biological markers of heavy alcohol consumption. [source]

Alcohol And Endothelial Function: A Brief Review

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2001
IB Puddey
SUMMARY 1. In spite of the dose-related effects of alcohol consumption to increase blood pressure, regular light to moderate alcohol intake appears to confer protection against both coronary artery disease and ischaemic stroke. In contrast, heavy alcohol consumption increases the risk of coronary artery disease and the risk of both haemorrhagic and ischaemic stroke. 2. Effects of alcohol consumption on endothelial cell function may be relevant to these disparate effects on cardiovascular outcomes. In in vitro animal studies, low doses of alcohol have been demonstrated to increase release of nitric oxide and augment endothelium-mediated vasodilatation, whereas higher doses impair endothelium-dependent relaxation responses. In contrast, chronic administration of alcohol to rats has generally been associated with tolerance to the acute inhibitory effects of alcohol on endothelium-mediated vasodilatation and may even result in augmentation of such responses. 3. The few human studies to date that have examined the effects of alcohol on endothelial function have focused on postischaemic flow-mediated dilation of the brachial artery (FMD). Although blunted FMD responses have been reported in alcoholic subjects, acute administration of alcohol or short-term interventions to reduce alcohol intake have had no effect to either improve or impair FMD. 4. Further studies in humans assessing acute and longer term dose-related effects of alcohol on endothelial function in both conduit and resistance vessels will be necessary if the relevance of the findings from in vitro and in vivo animal studies are to be understood in the context of the complex interrelationships of alcohol with cardiovascular disease. [source]