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Moderate Alcohol Consumption (moderate + alcohol_consumption)

Distribution by Scientific Domains

Medical Sciences	90%
Life Sciences	9%

Selected Abstracts

Moderate Alcohol Consumption in Later Life: Time for a Trial?

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 6 2009
Iain A. Lang PhD
No abstract is available for this article. [source]

Moderate Alcohol Consumption Suppresses Bone Turnover in Adult Female Rats

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 3 2001
R. T. Turner
Abstract Chronic alcohol abuse is a major risk factor for osteoporosis but the effects of moderate drinking on bone metabolism are largely uninvestigated. Here, we studied the long-term dose-response (0, 3, 6, 13, and 35% caloric intake) effects of alcohol on cancellous bone in the proximal tibia of 8-month-old female rats. After 4 months of treatment, all alcohol-consuming groups of rats had decreased bone turnover. The inhibitory effects of alcohol on bone formation were dose dependent. A reduction in osteoclast number occurred at the lowest level of consumption but there were no further reductions with higher levels of consumption. An imbalance between bone formation and bone resorption at higher levels of consumption of alcohol resulted in trabecular thinning. Our observations in rats raise the concern that moderate consumption of alcoholic beverages in humans may reduce bone turnover and potentially have detrimental effects on the skeleton. [source]

Relationship of Light to Moderate Alcohol Consumption and Risk of Hypertension in Japanese Male Office Workers

ALCOHOLISM, Issue 7 2002
Noriyuki Nakanishi
Background A close relationship between alcohol consumption and hypertension has been established, but the effect of light to moderate alcohol consumption on blood pressure (BP) remains unclear. Methods A total of 5275 Japanese male office workers aged 23 to 59 years partook in a survey. Subjects were classified as nondrinkers or current drinkers who averaged less than 12, 12 to 22, 23 to 45, or ,46 g/day of ethanol. BPs were measured at annual health examinations from May 1996 through May 2000. A total of 3784 hypertension-free (systolic BP <140 mm Hg, diastolic BP <90 mm Hg, no medication for hypertension, and no history of hypertension) men were observed for 4 years. Men in whom hypertension (systolic BP ,140 mm Hg, diastolic BP ,90 mm Hg, or both or receipt of antihypertensive medication) was found during repeated surveys were defined as incident cases of hypertension. Results After controlling for potential predictors of hypertension, systolic and diastolic BP levels and the incidence of hypertension were lowest in nondrinkers in all three age ranges (23,35, 36,47, and 45,59 years) and increased in a dose-dependent manner as alcohol consumption increased. For individuals aged 23 to 35 years, systolic and diastolic BP levels and the incidence of hypertension were significantly higher among those who drank an average of ,23 g/day of ethanol than among nondrinkers. For those aged 36 to 59, the diastolic BP level was significantly higher among those who drank any alcohol at all than among nondrinkers, and the systolic BP level and the incidence of hypertension were significantly higher among those who drank an average of ,12 g/day of ethanol than among nondrinkers. Conclusions Light to moderate alcohol consumption seems to have an important influence on BP in both young and middle-aged Japanese men. [source]

Alcohol-Induced Up-Regulation of Fibrinolytic Activity and Plasminogen Activators in Human Monocytes

ALCOHOLISM, Issue 8 2002
Edlue M. Tabengwa
Background Moderate alcohol consumption is associated with reduced risk for coronary heart disease. This may due, in part to increased fibrinolysis. Monocytes synthesize fibrinolytic proteins, tissue plasminogen activator (t-PA), urokinase plasminogen activator (u-PA), and their receptors. These studies were carried out to determine the effect of low alcohol on monocyte fibrinolytic activity and PA messenger RNA (mRNA) synthesis. Methods Peripheral blood monocytes and U937 cells were incubated in absence/presence of low alcohol (0.1%, v/v) for various times (0,1 hr), followed by incubations in the absence of alcohol (0,24 hr) before measurement of fibrinolytic activity and PA mRNA levels (reverse transcriptase polymerase chain reaction). Results Brief exposure (15 min, 4°C) of U937 cells to low alcohol resulted in an approximately 2- to 3-fold increase (269.0 ± 5.6 fmol/1 × 106 cells versus 656.0 ± 94.0 fmol/1 × 106 cells) in fibrinolytic activity. Preincubation of U937 cells and peripheral blood monocytes in low alcohol (1 hr, 37°C) followed by incubation in the absence of alcohol (24 hr) resulted in a sustained approximately 4- to 5-fold increase (414.0 ± 174.7 vs. 965.33.0 ± 104.8 fmol/1 × 106 cells) and an approximately 3- to 4-fold (20.5 ± 2.14 vs. 74 ± 2.28 fmol/2 × 106 cells, respectively) increase in fibrinolytic activity. Preincubation of monocytes with low alcohol (1 hr, 37°C) followed by incubation in the absence of alcohol (6 hr) resulted in an approximately 5- to 6-fold (0.06 ± 0.02 vs. 0.42 ± 0.02) and an approximately 2- to 3-fold (0.89 ± 0.04 vs. 2.07 ± 0.29) increase in t-PA and u-PA mRNA (reverse transcriptase polymerase chain reaction; PA/glyceraldehyde-3-phosphate dehydrogenase ratio), respectively. Conclusions These data suggest that low alcohol exerts a rapid, direct, and sustained effect on monocyte fibrinolytic activity, which may be, due in part, to increased monocyte t-PA/u-PA expression. These data provide a feasible molecular mechanism by which alcohol effects on monocyte fibrinolysis may contribute to the cardioprotective benefit associated with moderate alcohol consumption. [source]

Identification of a 251-bp Fragment of the PAI-1 Gene Promoter That Mediates the Ethanol-Induced Suppression of PAI-1 Expression

ALCOHOLISM, Issue 5 2001
Hernan E. Grenett
Background: Moderate alcohol consumption reduces the risk for coronary heart disease. This cardioprotection may be due to ethanol enhancement of fibrinolysis. Fibrinolysis involves the interaction of plasminogen activators (PAs) and the plasminogen activator inhibitor type-1 (PAI-1). Factor(s) that decrease endothelial cell (EC) PAI-1 expression increase fibrinolysis and may decrease the risk for cardiovascular disease. Methods: Five promoter deletion fragments were generated from a 1.1-kb PAI-1 promoter fragment and ligated to a luciferase reporter gene. Cultured human umbilical vein endothelial cells (HUVECs) were transiently transfected with these PAI-1 deletion constructs. A 251-base pair (bp) fragment of the PAI-1 promoter, positions ,800 to ,549, was cloned upstream of a heterologous promoter/enhancer. ECs luciferase activity was measured in the absence/presence of 20 mM ethanol. Electrophoresis mobility shift assays were performed with nuclear extracts from untreated and ethanol-treated ECs using this 251-bp fragment. Results: Deletion analysis showed a region between position ,800 and ,549 mediated ethanol repression of luciferase activity. This 251-bp promoter fragment also repressed the activity of a heterologous promoter/enhancer in the presence of ethanol. Using the labeled 251-bp fragment, nuclear extracts from ethanol-treated ECs contained two inducible bands and one enhanced band. Non-ethanol treated nuclear extracts also contained a band that was not observed in ethanol-treated samples. Competition using 100-fold molar excess of unlabeled probe abolished these four bands. Conclusions: Repression of PAI-I gene transcription in cultured HUVECs exposed to ethanol may involve the interaction of several transcription factors with binding sites localized between positions ,800 and ,549 of the PAI-1 gene promoter. [source]

Ethanol-Induced Up-Regulation of the Urokinase Receptor In Cultured Human Endothelial Cells

ALCOHOLISM, Issue 2 2001
Edlue M. Tabengwa
Background: Moderate alcohol consumption has been correlated to reduced coronary artery disease (CAD) risk and mortality. This alcohol effect may be mediated in part by an increased endothelial cell (EC) fibrinolysis. ECs synthesize fibrinolytic proteins, tissue plasminogen activator (t-PA), urokinase type plasminogen activator (u-PA), and plasminogen activator inhibitor type-1(PAI-1). In addition, they synthesize and regulate receptors for fibrinolytic proteins, namely (t-PA and plasminogen receptor) Annexin II and u-PA receptor (u-PAR). These receptors play an important role in the regulated expression of receptor-bound plasminogen activator conversion of receptor-bound plasminogen to receptor-bound plasmin on the EC surface (surface-localized fibrinolytic activity). Therefore, systemic factors, such as ethanol, that affect the level, or activity or interaction of one or more of these components, resulting in the increased expression of surface-localized EC fibrinolytic activity, will be expected to reduce the risk for thrombosis, CAD, and myocardial infarction (MI). We have previously shown that low ethanol up-regulates t-PA and u-PA gene transcription, while it down-regulates PAI-1, hence resulting in increased (sustained, 24 hr) surface-localized EC fibrinolytic activity. The current studies were carried out to determine whether low ethanol increased u-PAR expression in cultured human umbilical cord vein ECs (HUVECs). Methods: Cultured HUVECs were preincubated (1 hr) in the absence/presence of ethanol (0.025,0.2%, v/v); u-PAR mRNA (RT-PCR), antigen (western blot), and activity (125I-u-PA ligand binding/Scatchard analysis) levels were then measured after 0,24 hr. To determine whether the ethanol-induced changes in the u-PAR expression were transcriptional, transient transfection studies were carried out using a u-PAR/luciferase promoter construct (pu-PAR120/luc [1.2-kb u-PAR promoter fragment ligated to a promoterless luciferase vector]). Results: uPAR mRNA levels increased 2- to 3-fold and antigen levels (western blot) increased 2- to 4-fold while u-PA binding activity increased 36% (1.25 vs. 1.7 , 105 sites/cell, Bmax) without significantly affecting the Kd (1,2 nM). Transient transfection of cultured HUVECs with a pu-PAR120/luc construct resulted in a 2- to 3-fold increase in promoter activity in ethanol-induced cultures, compared with controls. Conclusion: These combined results demonstrate that low ethanol (,0.1%, v/v) induces the up-regulation of u-PAR gene transcription, resulting in increased u-PAR ligand binding activity. These results also further identify/define the contribution and role of another fibrinolytic protein in the overall ethanol-induced increase in surface-localized EC fibrinolysis that may underlie and contribute, in part, to the cardioprotection attributed to moderate alcohol consumption. [source]

Capillary zone electrophoresis with a dynamic double coating for analysis of carbohydrate-deficient transferrin in human serum: Impact of resolution between disialo- and trisialotransferrin on reference limits

ELECTROPHORESIS, Issue 24 2003
Christian Lanz
Abstract Capillary electrophoresis with a dynamic double coating formed by charged polymeric reagents represents a very effective tool for the separation of iron-saturated transferrin (Tf) isoforms and thus the determination of carbohydrate-deficient transferrin (CDT) in human serum. The resolution between di- and trisialo-Tf is dependent on the applied voltage and capillary temperature. With a 50 ,m inside diameter (ID) capillary of about 60 cm total length mounted into the P/ACE MDQ, 28 kV and 40°C, the resolution of the two Tf isoforms is shown to be between 1.0 and 1.4, whereas with reduced voltage and/or temperature, increased resolution at the expense of elongated run times is observed. Best data with complete resolution (Rs , 1.4) are obtained at 20 kV and 30°C. For the determination of CDT in serum, incomplete separation of di- and trisialo-Tf is demonstrated to have an impact on the reference limits. Analysis of the sera of 54 healthy individuals with no or moderate alcohol consumption and using valley-to-valley peak integration, the upper (lower) reference limits for CDT in relation to total Tf at the two power levels are 1.33 (0.52) and 1.57 (0.81)%, respectively, representing intervals that are significantly different (P < 0.001). Furthermore, the reference intervals are shown to be strongly dependent on the peak integration approach used. Valley-to-valley peak integration should only be employed for conditions with complete resolution between disialo- and trisialo-Tf. [source]

Alcohol drinking pattern and subjective health in a population-based study

ADDICTION, Issue 9 2006
Saverio Stranges
ABSTRACT Aims Some patterns of alcohol consumption (e.g. binge drinking, drinking outside of meals) have been associated with detrimental effects on health outcomes. Subjective health provides a global assessment of health status and is a strong predictor of total mortality; however, little is known about its relationship with alcohol drinking pattern. The association between several drinking patterns (i.e. drinking intensity and frequency, frequency of intoxication, drinking outside of meals, and beverage type) and subjective health was examined in a random sample of 3586 women and men. Design A population-based cross-sectional study. Methods Subjective health was assessed using the physical and mental health component summaries of the Short Form-36 health survey questionnaire. Alcohol consumption refers to the 30 days before the interview. Analysis of covariance compared gender-specific mean scores across alcohol drinking patterns. Findings Overall, non-current drinkers reported poorer physical and mental health than life-time abstainers and current drinkers, while no consistent differences were found between life-time abstainers and current drinkers. In female current drinkers, daily drinking, beer and mixed beverage consumption were associated with better mental health. In male current drinkers, moderate alcohol consumption (2,2.9 drinks per day), wine and mixed beverage consumption were associated with better physical health. Intoxication and liquor consumption were associated with poorer mental health in women and poorer physical health in men. No consistent associations were found for drinking outside meals. Conclusions Aspects of drinking pattern may affect subjective health differentially in women and men. Overall, intoxication and liquor drinking are associated with poorer self-perceived health status than regular, moderate consumption of other alcoholic beverages. [source]

Abstention, alcohol use and risk of myocardial infarction in men and women taking account of social support and working conditions: the SHEEP case,control study

ADDICTION, Issue 10 2003
Anders Romelsjö
ABSTRACT Aims, Very few studies indicating that low,moderate alcohol consumption protects from myocardial infarction (MI) controlled for social support and working conditions, which could confound the findings. Therefore, a first aim was to study the risk of non-fatal and total MI in relation to volume of alcohol consumption and measures of social support and working conditions. A second aim was to analyse the impact of the volume of earlier alcohol use in abstainers. Design, Data came from a case,control study, the Stockholm Heart Epidemiology Program (SHEEP), including first MI among Swedish citizens 45,70 years old. Setting, Stockholm County 1992,94. Participants, There were 1095 cases of MI in men and 471 in women (928 and 372 were non-fatal), and 2339 living controls from the general population. Measurement, Information about alcohol use at different periods in life and job strain, social anchorage and life control besides pre-existing health problems, smoking, physical activity, socio-economic status and marital status was obtained by a questionnaire from the cases and the controls. Findings, In multivariate logistic regression analyses, the relative risk for MI (especially non-fatal) was reduced among alcohol consumers. RR for non-fatal MI was 0.52 (95% confidence intervals 0.32, 0.85) in men with a consumption of 50,69.9 g 100% ethanol/day and 0.21 (95% confidence interval 0.06, 0.77) in women with a consumption of 30 g or more per day (reference category 0.1,5 g 100% ethanol/day). Men who were abstainers during the previous 1,10 years and with an earlier average consumption of 5,30 g 100% ethanol/day had a significantly lower relative risk compared to such abstainers with an earlier higher consumption. Earlier consumption among abstainers may also have an impact on gender differences in MI. Analyses showed positive interaction between abstention and low life-control in women, but only 4% of the female cases were due to this interaction. There were no other interactions between measures of alcohol use and social anchorage, life control and working situations. Conclusion, Alcohol use had a protective impact on MI, with little impact of job strain, social anchorage and life control, giving increased support for a protective impact of low-moderate alcohol use. The level of previous alcohol consumption among male 1,10-year-long abstainers influenced the risk of MI. [source]

Alcohol consumption increases attractiveness ratings of opposite-sex faces: a possible third route to risky sex

ADDICTION, Issue 8 2003
Barry T. Jones
ABSTRACT Aims, To measure the effect of moderate alcohol consumption on males' and females' attractiveness ratings of unfamiliar male and female faces. Participants Eighty undergraduate volunteers were used in each of three experiments. Design, Participants' ratings on a 1,7 scale was the dependent variable. A three-factor mixed design was used. For experiments 1 and 2: one within-factor, sex-of-face to be rated (male/female); two between-factors, sex-of-rater (male/female) and alcohol status of rater (0 UK units/1,6 UK units). For experiment 3, the two levels of sex-of-face were replaced by two levels of a non-face object. In experiment 1, the faces were rated for attractiveness; in experiment 2, the faces were rated for distinctiveness and in experiment 3, the non-face objects were rated for attractiveness. Setting, Quiet, prepared corners of bars and licensed eating areas on a civic university campus. Method, For each experiment, 118 full-colour photographic images were presented randomly on a laptop computer screen, each remaining until a rating response was made. Findings, There was a significant alcohol consumption enhancement effect only for attractiveness ratings of opposite-sex faces in experiment 1. This indicates that the opposite-sex enhancement effect is not due simply to alcohol consumption causing the use of higher points of ratings scales, in general. Conclusion, Since Agocha & Cooper have shown that the likelihood of intentions to engage in risky sex increases as the facial attractiveness of the potential sexual partner increases, through the opposite-sex enhancement effect we identify a new possible link between risky sex and alcohol consumption. [source]

Alcohol inflammation and coronary heart disease

ADDICTION BIOLOGY, Issue 3 2003
ARMIN IMHOF
This overview summarizes the experimental and epidemiological evidence linking alcohol consumption and the immune system. It focuses on findings supporting the notion that moderate alcohol consumption exerts anti-inflammatory effects which may explain, at least in part, the reduced risk of coronary heart disease morbidity and mortality in these subjects. Alcohol consumption has been shown consistently to be associated with all-cause mortality in a J- or U-shaped manner. This is due primarily to reduced risk of coronary heart disease (CHD) mortality among moderate consumers of alcohol compared to abstainers and heavy drinkers. Several mechanisms have been suggested by which moderate alcohol consumption could lower risk of CHD. However, changes in lipids, such as increased HDL cholesterol and apolipoprotein A1 or a favourable haemostatic profile, can only partly explain the beneficial effects. Recently, anti-inflammatory effects of moderate intake of alcohol have been considered as an additional possible explanation, as inflammation has a fundamental role in the initiation, progression and the thrombotic complications of atherosclerosis. [source]

Moderate Alcohol Consumption Aggravates High-Fat Diet Induced Steatohepatitis in Rats

ALCOHOLISM, Issue 3 2010
Yan Wang
Background:, Nonalcoholic steatohepatitis (NASH) develops in the absence of chronic and excessive alcohol consumption. However, it remains unknown whether moderate alcohol consumption aggravates liver inflammation in pre-existing NASH condition. Methods:, Sprague-Dawley rats were first fed ad libitum with Lieber-DeCarli high-fat diet (71% energy from fat) for 6 weeks to induce NASH, as demonstrated previously. Afterwards, these rats were continuously fed with high-fat diet (HFD, 55% total energy from fat) or high fat plus alcohol diet (HFA, 55% energy from fat and 16% energy from alcohol) for an additional 4 weeks. Pathological lesions including fat accumulation and inflammatory foci in liver were examined and graded. Lipid peroxidation and apoptotic hepatocytes in the liver were assessed. The mRNA expressions of tumor necrosis factor-, (TNF,) and TNF receptor 1 (TNF-R1), Fas death receptor (Fas) and Fas ligant (FasL), IL-1, and IL-12 were determined by real-time PCR. Protein levels of total and cleaved caspase-3, CYP2E1, Bax, and Bcl-2 were measured by western blotting. Results:, The number of hepatic inflammatory foci and apoptotic hepatocytes were significantly increased in rats fed with HFA as compared with those in HFD-fed rats. The aggravated inflammatory response and cellular apoptosis mediated by HFA were associated with elevated mRNA expression of Fas/FasL and cleaved caspase-3 protein. Although no significant differences were observed between HFD and HFA groups, the levels of lipid peroxidation, Bax and Bcl-2 protein concentration, and mRNA levels of other inflammatory cytokines were significantly higher in these 2 groups than those in the control group. Conclusions:, These data suggest that even moderate alcohol consumption can cause more hepatic inflammation and cellular apoptosis in a pre-existing NASH condition. [source]

Alcohol in Moderation, Cardioprotection, and Neuroprotection: Epidemiological Considerations and Mechanistic Studies

ALCOHOLISM, Issue 2 2009
Michael A. Collins
In contrast to many years of important research and clinical attention to the pathological effects of alcohol (ethanol) abuse, the past several decades have seen the publication of a number of peer-reviewed studies indicating the beneficial effects of light-moderate, nonbinge consumption of varied alcoholic beverages, as well as experimental demonstrations that moderate alcohol exposure can initiate typically cytoprotective mechanisms. A considerable body of epidemiology associates moderate alcohol consumption with significantly reduced risks of coronary heart disease and, albeit currently a less robust relationship, cerebrovascular (ischemic) stroke. Experimental studies with experimental rodent models and cultures (cardiac myocytes, endothelial cells) indicate that moderate alcohol exposure can promote anti-inflammatory processes involving adenosine receptors, protein kinase C (PKC), nitric oxide synthase, heat shock proteins, and others which could underlie cardioprotection. Also, brain functional comparisons between older moderate alcohol consumers and nondrinkers have received more recent epidemiological study. In over half of nearly 45 reports since the early 1990s, significantly reduced risks of cognitive loss or dementia in moderate, nonbinge consumers of alcohol (wine, beer, liquor) have been observed, whereas increased risk has been seen only in a few studies. Physiological explanations for the apparent CNS benefits of moderate consumption have invoked alcohol's cardiovascular and/or hematological effects, but there is also experimental evidence that moderate alcohol levels can exert direct "neuroprotective" actions,pertinent are several studies in vivo and rat brain organotypic cultures, in which antecedent or preconditioning exposure to moderate alcohol neuroprotects against ischemia, endotoxin, ,-amyloid, a toxic protein intimately associated with Alzheimer's, or gp120, the neuroinflammatory HIV-1 envelope protein. The alcohol-dependent neuroprotected state appears linked to activation of signal transduction processes potentially involving reactive oxygen species, several key protein kinases, and increased heat shock proteins. Thus to a certain extent, moderate alcohol exposure appears to trigger analogous mild stress-associated, anti-inflammatory mechanisms in the heart, vasculature, and brain that tend to promote cellular survival pathways. [source]

Effects of a Moderate Evening Alcohol Dose.

ALCOHOLISM, Issue 8 2007
I: Sleepiness
Background: Few studies examining alcohol's effects consider prior sleep/wake history and circadian timing. We examined introspective and physiological sleepiness on nights with and without moderate alcohol consumption in well-rested young adults at a known circadian phase. Methods: Twenty-nine adults (males=9), ages 21 to 25 years (M=22.6, SD=1.2), spent 1 week on an at-home stabilized sleep schedule (8.5 or 9 hours), followed by 3 in-lab nights: adaptation, placebo, and alcohol. Alcohol (vodka; 0.54 g/kg for men; 0.49 g/kg for women) or placebo beverage was consumed over 30 minutes ending 1 hour before stabilized bedtime. In addition to baseline, 3 sleep latency tests (SLTs) occurred after alcohol/placebo ingestion (15, 16.5, and 18 hours after waking). Stanford Sleepiness Scales (SSS) and Visual Analog Scales (VAS) of sleepiness were completed before each SLT and approximately every 30 minutes. The Biphasic Alcohol Effects Scale (BAES) was administered a total of 4 times (baseline, 5, 60, and 90 minutes postalcohol/placebo). Subjects' circadian phase was determined from melatonin levels in saliva samples taken at approximately 30-minute intervals. Results: All sleepiness and sedation measures increased with time awake. Only SSS and BAES sedation measures showed higher levels of sleepiness and sedation after alcohol compared with placebo. The mean circadian phase was the same for assessments at both conditions. Conclusions: Alcohol did not increase physiological sleepiness compared with placebo nor was residual sedation evident under these conditions. We conclude that the effects on sleepiness of a moderate dose of alcohol are masked when sleep,wake homeostatic and circadian timing influences promote high levels of sleepiness. [source]

Effects of Alcohol on Polysomnographically Recorded Sleep in Healthy Subjects

ALCOHOLISM, Issue 9 2006
Bernd Feige
Background: After studying the sleep of alcohol-dependent patients at the beginning and over the course of abstinence in earlier studies, our interest in the current study focused on the direct effect of 2 doses of alcohol [0.03 and 0.1% blood alcohol level (BAL)] on healthy sleep. This is the first polysomnographic study testing the impact of 2 doses of alcohol ingestion (thus reflecting "normal" social drinking and alcohol abuse) in a single-blind randomized design in healthy volunteers. The study evaluated a short-term acute drinking period for 3 and 2 days of withdrawal from alcohol not only for polysomnographic variables but also for subjective estimates of sleep quality. Methods: In a crossover design with a 1-week interval, healthy subjects received alcohol to raise their blood alcohol to either 0.03 or 0.1% BAL at bedtime for 3 consecutive nights after an alcohol-free baseline night. Objective (polysomnography) and subjective sleep (questionnaires) was recorded each night. During the following 2 days, alcohol was discontinued with simultaneous measurements of sleep to gauge withdrawal effects. Results: At a dose of alcohol leading to BAL of 0.03%, no clear effects could be detected. Following an evening BAL of 0.1%, a hypnotic-like effect (shortened sleep latency, reduced number of wake periods, decreased stage 1 sleep) occurred primarily during the first half of the night with signs of rebound effects being already present during the second half of the night (increased stage 1 sleep). At this dose, alcohol significantly increased slow-wave sleep (SWS) in the first half of the night and reduced REM density in the beginning of the night. After discontinuation of the higher alcohol dose, REM sleep amount increased. No significant withdrawal or rebound effects could be observed for parameters of sleep continuity during the 2 nights after discontinuation from alcohol at a BAL of 0.1%. Conclusions: Owing to the small sample size, the results of this study need to be interpreted with caution. Short-term moderate alcohol consumption (BAL 0.03%) did not significantly alter objective or subjective parameters of sleep. Higher doses of alcohol resulting in a BAL level of 0.10% immediately before going to bed mainly influenced sleep in the first half of the night, resembling the effects of a short-acting hypnotic drug, including a suppression of phasic aspects of REM sleep (REM density). Interestingly, analysis of the latter part of these nights indicated the immediate presence of withdrawal effects (increased light sleep). No statistically significant effects on sleep parameters were observable during the 2 nights of withdrawal from alcohol at the higher BAL. Interpreted carefully, our data indicate that negative effects on sleep occur already with short-term use of alcohol at doses of BAL of 0.10%, despite hypnotic-like effects during the first hours of sleep, especially during the latter part of the night. [source]

Moderate Alcohol Intake in Humans Attenuates Monocyte Inflammatory Responses: Inhibition of Nuclear Regulatory Factor Kappa B and Induction of Interleukin 10

ALCOHOLISM, Issue 1 2006
Pranoti Mandrekar
Background: In contrast to the deleterious effects of chronic excessive alcohol consumption on the liver and cardiovascular system, modest alcohol intake, such as 1 to 2 drinks per day, has benefits on cardiovascular mortality. Little is known about the length of time or the amounts of alcohol consumed that may cause alterations in inflammatory cells such as monocytes that are crucial to atherosclerotic vascular disease. Here, we determine in vivo effects of acute alcohol consumption on inflammatory cytokine production and nuclear regulatory factor ,B (NF- ,B) binding in human monocytes. Methods: Human blood monocytes were isolated by plastic adherence before and after acute alcohol consumption (2 ml vodka/kg body weight). Lipopolysaccharide (LPS)- and superantigen-induced tumor necrosis factor , (TNF ,), interleukin (IL)-1,, and IL-10 production were then determined in monocytes by ELISA. Nuclear regulatory factor- ,B activity of monocytes before and after alcohol consumption was estimated by electromobility shift assay and promoter-driven reporter activity. I,B, was determined by Western blotting in the cytoplasmic extracts. Results: Eighteen hours after moderate alcohol consumption, we found a significant reduction in monocyte production of inflammatory mediators, TNF- , and IL-1,, in response to LPS or staphylococcal enterotoxin B stimulation. Acute alcohol consumption inhibited LPS-induced DNA binding of the p65/p50 NF- ,B in monocytes that regulates the expression of both the TNF- , and the IL-1, genes. Consistent with this, acute alcohol treatment (25 mM) significantly reduced LPS-induced activation of an NF- ,B-driven reporter gene suggesting inhibition of this proinflammatory signaling pathway. Further, LPS-induced I,B, degradation was not affected by acute alcohol consumption indicating an I,B, -independent mechanism, as observed earlier in the in vitro acute alcohol studies. In contrast, monocyte production of the anti-inflammatory cytokine, IL-10, was augmented by acute alcohol intake. Conclusions: Our findings suggest that acute alcohol consumption has dual anti-inflammatory effects that involve augmentation of IL-10 and attenuation of monocyte inflammatory responses involving inhibition of NF- ,B. These mechanisms may contribute to the beneficial effects of moderate alcohol use on atherosclerosis. [source]

Alcohol-Induced Up-Regulation of Fibrinolytic Activity and Plasminogen Activators in Human Monocytes

Ethanol-Induced Up-Regulation of Candidate Plasminogen Receptor Annexin II in Cultured Human Endothelial Cells

ALCOHOLISM, Issue 6 2000
Edlue M. Tabengwa
Introduction Epidemiological studies indicate that moderate alcohol consumption reduces the risk for coronary heart disease and that this cardioprotective benefit may be mediated, in part, by increased fibrinolysis. Endothelial cells (ECs) synthesize plasminogen activators, tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), receptors for plasminogen activators, and a receptor for plasminogen, annexin II (Ann-II). These receptors localize and facilitate receptor-bound plasminogen activator-mediated conversion of receptor-bound plasminogen to receptor-bound plasmin on the EC surface, which results in the regulated expression of surface-localized EC fibrinolytic activity. Ethanol is a systemic factor that affects these components, which increases EC fibrinolysis and hence reduces the risk for thrombosis, coronary heart disease, and myocardial infarction (MI). Methods: This study was carried out to determine whether low ethanol (0.1% v/v) increased plasminogen receptor, Ann-II antigen (western blot), messenger ribonucleic acid (mRNA) (reverse transcription polymerase chain reaction; RT-PCR) expression, activity (ligand binding/Scatchard analysis), and hence fibrinolysis (plasmin generation) in cultured human ECs. Results: Plasminogen receptor activity increased ,2-fold (2.5 vs. 5.6 × 106 sites/cell), as evidenced by increased 125I-labeled Glu-plasminogen ligand binding/Scatchard analysis. In addition, western blot analyses indicated an increase in Ann-II antigen, and mRNA levels increased ,2-fold (RT-PCR). This increase in Ann-II expression was concomitant with ,2- to 3-fold sustained increase (,24 hr) in surface-localized EC fibrinolytic activity. Nuclear transcription run-on assays showed an ,5- to 6-fold increase in new 32P-labeled Ann-II mRNA levels, compared with controls (no ethanol). Conclusions: These results demonstrated that low ethanol increased Ann-II antigen/mRNA levels and up-regulated Ann-II gene expression at the transcriptional level. The results further identify and define the contribution and role of the plasminogen receptor, Ann-II, in the ethanol-induced mechanism of increased EC fibrinolysis that may underlie and contribute, in part, to the cardioprotective benefit associated with moderate alcohol consumption. [source]

Genetic variation in alcohol dehydrogenase 3 and the decrease of hs-C-reactive protein levels by moderate alcohol consumption

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 4 2005
K. FURMAN
No abstract is available for this article. [source]

Moderate alcohol intake increases fibrosis progression in untreated patients with hepatitis C virus infection

JOURNAL OF VIRAL HEPATITIS, Issue 3 2002
J. Westin
Although excessive alcohol consumption in combination with hepatitis C virus (HCV) infection is known to increase the risk of liver cirrhosis, the effect of moderate alcohol intake remains to be elucidated. The aim of this study was to evaluate the effect of moderate alcohol consumption on fibrosis progression in HCV infection. A group of 78 patients with HCV infection and moderate alcohol consumption were analysed retrospectively. All patients had undergone two liver biopsies, with a median time between biopsies of 6.3 years, and had not received any antiviral therapy. Their lifetime drinking history was recorded. All patients except one had daily alcohol consumption below 40 g of ethanol (median 4.8 g/day, interquartile range 1.1,11.6 g/day) during the period between the biopsies. The patients whose liver fibrosis had deteriorated had a higher total alcohol consumption and higher drinking frequency between the biopsies. The degree of fibrosis progression was greater in patients with a total alcohol intake and drinking frequency above the median level for the group. A multiple logistic regression analysis showed that drinking frequency and time between biopsies were independently associated with fibrosis progression. Hence, even moderate alcohol intake seems to increase fibrosis progression in HCV-infected patients. From that point of view, total abstention ought to be recommended. If this is not achieved, occasional use of alcohol is probably less harmful than daily drinking for patients with low or moderate alcohol consumption. [source]

Moderate wine consumption is associated with better cognitive test results: a 7 year follow up of 5033 subjects in the Tromsø Study

ACTA NEUROLOGICA SCANDINAVICA, Issue 2010
K. A. Arntzen
Arntzen KA, Schirmer H, Wilsgaard T, Mathiesen EB. Moderate wine consumption is associated with better cognitive test results: a 7 year follow up of 5033 subjects in the Tromsø Study. Acta Neurol Scand: 2010: 122 (Suppl. 190): 23,29. © 2010 John Wiley & Sons A/S. Background,,, The impact of moderate alcohol consumption on cognitive function and dementia is unclear. We examined the relationship between consumption of different alcoholic beverages and cognitive function in a large population-based study. Methods,,, Subjects were 5033 stroke-free men and women who participated in a longitudinal population-based study in Tromsø, Norway. Alcohol consumption and other cardiovascular risk factors were measured at baseline and cognitive function was assessed after 7 years follow up with verbal memory test, digit,symbol coding test and tapping test. Results,,, Moderate wine consumption was independently associated with better performance on all cognitive tests in both men and women. There was no consistent association between consumption of beer and spirits and cognitive test results. Alcohol abstention was associated with lower cognitive performance in women. Conclusions,,, Light-to-moderate wine consumption was associated with better performance on cognitive tests after 7 years follow up. [source]