Effects Of Acute Alcohol Consumption Research Articles

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

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 kappaB (NF-kappaB) binding in human monocytes. 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 alpha (TNF alpha), interleukin (IL)-1beta, and IL-10 production were then determined in monocytes by ELISA. Nuclear regulatory factor-kappaB activity of monocytes before and after alcohol consumption was estimated by electromobility shift assay and promoter-driven reporter activity. IkappaBalpha was determined by Western blotting in the cytoplasmic extracts. Eighteen hours after moderate alcohol consumption, we found a significant reduction in monocyte production of inflammatory mediators, TNF-alpha and IL-1beta, in response to LPS or staphylococcal enterotoxin B stimulation. Acute alcohol consumption inhibited LPS-induced DNA binding of the p65/p50 NF-kappaB in monocytes that regulates the expression of both the TNF-alpha and the IL-1beta genes. Consistent with this, acute alcohol treatment (25 mM) significantly reduced LPS-induced activation of an NF-kappaB-driven reporter gene suggesting inhibition of this proinflammatory signaling pathway. Further, LPS-induced IkappaBalpha degradation was not affected by acute alcohol consumption indicating an IkappaBalpha-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. 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-kappaB. These mechanisms may contribute to the beneficial effects of moderate alcohol use on atherosclerosis.

The effects of acute alcohol consumption, cognitive reserve, partner risk, and gender on sexual decision making.

In past alcohol administration studies, intoxicated college students have been more willing to have unprotected sex with a hypothetical new partner than sober or placebo students. The objective of the present research was to extend past work by examining the effects of gender, cognitive reserve, and partner risk on intoxicated sexual decision making. Before assigning participants (60 women and 60 men) to a drink condition, cognitive reserve was assessed with the reading subtest of the Wide Range Achievement Test 3 (WRAT3). After drinking, participants watched a video of a male and female college student in a sexual situation. There were two versions of the video that were identical, except for information that suggested the opposite-gender character had many past sexual partners or only a few. There was a significant interaction between drink condition and cognitive reserve such that intoxicated participants with lower WRAT3 scores were more likely than other participants to indicate that they would have unprotected sex if they were in this situation. Partner risk did not influence participants' willingness to have unprotected sex; however, they were less interested in dating the high-risk partner. As expected, participants with less cognitive reserve made riskier decisions when intoxicated. Unexpectedly, although participants clearly perceived the high- and low-risk partners differently, this did not affect their willingness to have unprotected sex with this hypothetical partner. These findings demonstrate the need for sexually transmitted disease/ HIV prevention programs that go beyond factual presentations and provide students with the skills they need to assess risk realistically and the need for programs with messages tailored for individuals with low cognitive skills.

THE RELATIONSHIP BETWEEN ACUTE ALCOHOL CONSUMPTION AND CONSEQUENT INJURY TYPE

The aim of this study was to quantify the relationship between acute alcohol consumption and injury type (nature of injury, body region injured), while adjusting for the effect of known confounders (i.e. demographic and situational variables, usual drinking patterns, substance use and risk-taking behaviour). A cross-sectional study was conducted between October, 2000 and October, 2001 of patients aged >or=15 years presenting to a Queensland Emergency Department for treatment of an injury sustained in the preceding 24 h. There were three measures of acute alcohol consumption: drinking setting, quantity, and beverage type consumed in the 6 h prior to injury. Two variables were used to quantify injury type: nature of injury (fracture/dislocation, superficial, internal, and CNS injury) and body part injured (head/neck, facial, chest, abdominal, external, and extremities). Both were derived from patient medical records. Five hundred and ninety three patients were interviewed. Logistic regression analyses indicated that, after controlling for relevant confounding variables, there was no significant association between any of the three measures of acute alcohol consumption and injury type. The effects of acute alcohol consumption are not specific to injury type. Interventions aimed at reducing the incidence of alcohol-related injury should not be targeted at specific injury types.

The cumulative effects of acute alcohol consumption, individual differences and situational perceptions on sexual decision making.

Past alcohol administration research has produced mixed findings regarding the role of acute alcohol consumption on sexual decision making. The purpose of this study was to evaluate a more complex theoretical model that places alcohol's acute effects in context, through the inclusion of background measures as well as affective and cognitive responses to the specific situation. College students (90 men, 90 women) completed a survey that included measures of individual difference characteristics and past experiences; approximately 1 month later, they participated in an alcohol administration study. Participants were randomly assigned to one of three drink conditions (sober, placebo, alcohol), after which they read a story about a couple that wanted to have sex, but had no condoms available. In hierarchical multiple regression analyses, acute alcohol consumption significantly predicted participants' perceived likelihood that they would have sex without a condom in such a situation; an earlier step included gender, impulsivity, self-reported alcohol expectancies, frequency of heavy drinking, lifetime number of sexual partners and frequency of condom use. There was no significant effect associated with the expectancy that one had consumed alcohol. Neither was there a significant interaction between drink condition and self-reported alcohol expectancies. Through the inclusion of measures of individual differences and responses to the specific situation, this study provides a more nuanced understanding of the factors that affect college students' sexual decision making, compared with laboratory studies that examine the effects of acute alcohol consumption in isolation. Alcohol consumption explained a significant yet relatively small amount of variance. Researchers need to consider the broader context to understand how intoxication influences sexual decision making.

106-LOOKING FOR NEW STRESS MEASURES-ALPHA-AMYLASE IN SALIVA

Objective: The aim of our study was to evaluate the effects of acute alcohol consumption on saliva secretion rate and selected salivary parameters in healthy nonalcoholic volunteers. Study Design: Twenty-four volunteers (37.7 ± 9.6 years, mean ± SD) consumed 0.6 g or 0.7 g alcohol/kg of body weight (for women and men, respectively) in a soft drink. Saliva samples were collected, first (S0) before any alcohol was consumed, 45 minutes after consumption (S1) and, finally, 60 minutes after S1 (S2). Flow rates of both resting whole saliva and paraffin-stimulated (SWS) whole saliva were assessed. SWS was assessed for amylase, total protein, inorganic phosphate (PO43–), sodium (Na+), potassium (K+), and calcium (Ca2+) content. Results: SWS, but not resting whole saliva (in milliliters/minute), decreased significantly after consumption of alcohol. Amylase activity (P =.010) and the concentrations of Na+ (P =.000) and Ca2+ (P =.002) decreased significantly between S0 and S1. When SWS was analyzed for output, the total protein concentration (S0 to S1, P =.000; S0 to S2, P =.033) and amylase activity (S0 to S1, P =.000) decreased significantly. Further, the output of all the studied electrolytes decreased significantly as blood alcohol concentration increased. Conclusions: We conclude that acute alcohol consumption causes a decrease in SWS flow rate. The decrease in flow rate also results in impaired output of total protein and amylase, as well as in a decrease in the output of electrolytes.(Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92:292-8)

Binge ethanol exposure increases liver injury in obese rats

Background & Aims : The objective of this study was to address the hepatic effects of acute alcohol consumption in obesity by simulating an alcohol binge in genetically obese fa/fa rats compared with lean Fa/? rats. Methods : Ethanol 4 g/kg or saline was administered by gavage every 12 hours for 3 days. Results : Plasma alcohol levels were similar in both groups. Binge ethanol exposure caused liver injury in obese fa/fa but not in lean Fa/? rats, as assessed by alanine aminotransferase and H&E staining. Obesity impaired the antioxidant defense because basal levels of glutathione, glutamate cysteine ligase modulatory subunit, catalase, glutathione reductase, and superoxide dismutase were lower in fa/fa compared with Fa/? rats; the ethanol binge further decreased these antioxidants in fa/fa rats and also decreased glutathione peroxidase activity. Nonesterified fatty acids and lipid peroxidation were increased after ethanol treatment in fa/fa rats. Cytochrome P450 2E1 was down-regulated in fa/fa compared with Fa/? rats; however, the ethanol binge increased cytochrome P450 2E1 in both genotypes. Adenosine triphosphate decreased and uncoupling protein 2 increased in fa/fa rats treated with ethanol. 3-Nitrotyrosine protein adducts were detected only in fa/fa rats treated with ethanol, and this was accompanied by an induction of inducible nitric oxide synthase. Ethanol binge increased caspase-3 and caspase-8 activity, the expression of Fas ligand, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling in fa/fa rats. Conclusions : These data indicate that binge drinking increases apoptosis and liver injury in obese rats more than in lean controls and suggest that the injury may involve oxidative and nitrosative damage.

Acute Effects of Alcohol on Auditory Thresholds and Distortion Product Otoacoustic Emissions in Humans

Objective—To investigate the acute effects of alcohol consumption on pure-tone thresholds (PTs) and distortion product otoacoustic emissions (DPOAEs) in humans.Material and Methods—Eight healthy adults were asked to drink alcohol to the clinical intoxication level. PTs and DPOAEs were determined serially before and after alcohol ingestion.Results—Alcohol had no effect on PTs. DPOAE amplitudes above 5500 Hz dropped 30 min and 1 h after alcohol ingestion, returning to the pre-test level 2 h after ingestion.Conclusion—In humans, acute alcohol consumption to the intoxication level may cause a temporary reduction in DPOAE amplitudes at high frequencies without affecting auditory thresholds.

Saliva flow rate, amylase activity, and protein and electrolyte concentrations in saliva after acute alcohol consumption.

The aim of our study was to evaluate the effects of acute alcohol consumption on saliva secretion rate and selected salivary parameters in healthy nonalcoholic volunteers. Twenty-four volunteers (37.7 +/- 9.6 years, mean +/- SD) consumed 0.6 g or 0.7 g alcohol/kg of body weight (for women and men, respectively) in a soft drink. Saliva samples were collected, first (S0) before any alcohol was consumed, 45 minutes after consumption (S1) and, finally, 60 minutes after S1 (S2). Flow rates of both resting whole saliva and paraffin-stimulated (SWS) whole saliva were assessed. SWS was assessed for amylase, total protein, inorganic phosphate (PO4(3-)), sodium (Na+), potassium (K+), and calcium (Ca2+) content. SWS, but not resting whole saliva (in milliliters/minute), decreased significantly after consumption of alcohol. Amylase activity (P =.010) and the concentrations of Na+ (P =.000) and Ca2+ (P =.002) decreased significantly between S0 and S1. When SWS was analyzed for output, the total protein concentration (S0 to S1, P =.000; S0 to S2, P =.033) and amylase activity (S0 to S1, P =.000) decreased significantly. Further, the output of all the studied electrolytes decreased significantly as blood alcohol concentration increased. We conclude that acute alcohol consumption causes a decrease in SWS flow rate. The decrease in flow rate also results in impaired output of total protein and amylase, as well as in a decrease in the output of electrolytes.

Alcohol and visual performance

1. 1. The authors examined the effect of acute alcohol consumption on a set of visual tasks: visual short term memory, depth perception and attention. 2. 2. In a repeated measurement design, thirteen subjects performed the tasks once sober and once intoxicated with 0.8 g/kg body weight pure ethanol in orange juice (33% alcohol). Subjects underwent a neuropsychological (Benton test) and a psychophysical test (vernier discrimination) both assessing visual short term memory, the test d2 as a measure of attention and concentration and a psychophysical depth perception task. 3. 3. Subjects demonstrated significant alcohol-related impairments in depth perception and in visual short term memory as assessed by the vernier discrimination task. However, the neuropsychological Benton test and test d2 failed to reveal alcoholrelated changes in performance — probably due to superimposed learning effects. Performance was neither correlated with blood alcohol levels (BAL) nor perceived intoxication. Even though the current BAL was known to the subjects, only half of them demonstrated a close correlation between BAL and perceived intoxication.

Alcohol-Induced Stimulation and Sedation: Relation to Physical Aggression

The relation between the stimulating and the sedating effects of acute alcohol consumption on human physical aggression was examined. Sixty male social drinkers were assigned to either an alcohol or a sober group. Aggression was measured using a modified version of S. Taylor's (1967) aggression paradigm, in which electric shocks are received from and administered to a fictitious opponent during a competitive task. Aggression was operationalized as the intensity and the duration of the shocks selected. Stimulation and sedation were measured using a self-report inventory. Results demonstrated that stimulation was positively related to aggression, but only in the intoxicated state. Sedation was not related to aggression in either the intoxicated or the sober state.

Pathogenetic Mechanisms of Hypomagnesemia in Alcoholic Patients

The aim of our study was to describe the possible pathophysiologic mechanisms of hypomagnesemia in alcoholic patients. A total of 127 chronic alcoholic patients admitted to our university hospital for causes related to alcohol abuse were studied. Hypomagnesemia was the most common electrolyte disturbance observed in 38 patients (29.9%). In 18 of them inappropriate magnesiuria was evident, possibly due to hypophosphatemia, to metabolic acidosis or to a direct magnesiuric effect of acute alcohol consumption. The causes of hypomagnesemia in the remaining 20 patients were alcohol withdrawal syndrome and diarrhea. Respiratory alkalosis was evident in 10 hypomagnesemic patients and could have played a role in the development of hypomagnesemia. A decreased magnesium intake could also have contributed to the hypomagnesemia, especially in malnourished alcoholic patients. Hypomagnesemic patients more frequently had other acid-base and electrolyte abnormalities, such as hypophosphatemia, hypokalemia, hypocalcemia, and respiratory alkalosis, as compared with the normomagnesemic patients. Moreover, in hypomagnesemic patients serum magnesium levels were correlated with the indices of potassium and phosphorus excretion, suggesting that serum magnesium levels play a central role in the homeostasis of the other electrolytes. In conclusion, hypomagnesemia is the most common electrolyte abnormality observed in alcoholic patients, as a result of various pathophysiologic mechanisms.

Effects of alcohol consumption on pharmacokinetics, efficacy, and safety of fluvastatin

<h2>Abstract</h2> Alcohol consumption is known to have beneficial effects on cardiac mortality, probably by increasing high density lipoprotein cholesterol (HDL-C). Alcohol also increases triglycerides and, in some studies, total cholesterol and low density lipoprotein cholesterol (LDL-C). Nothing is known, however, of the effects of alcohol on the pharmacokinetics and efficacy of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors. Consequently, 2 studies have been carried out to determine the effects of alcohol consumption on the pharmacokinetics and efficacy of the HMG-CoA reductase inhibitor fluvastatin. Firstly, the effects of acute alcohol consumption on a single, oral 40 mg dose of fluvastatin were examined in a reference-controlled, randomized, crossover study in 10 healthy volunteers. Measurements were made after ingestion of 70 g of ethanol diluted to 20% with lemonade and, following a 7-day period, after ingestion of lemonade alone (reference). The half-life (<i>t</i>_1/2) of a single dose of fluvastatin was significantly reduced by acute alcohol consumption compared with reference, whereas the area under the time—concentration curve (AUC), peak concentration (<i>C</i>_max), and time to peak concentration (<i>t</i>_max) did not differ from the reference group. The lipid profile, measured 8 hr after administration, did not differ significantly from baseline in the reference group, apart from a slight reduction in apolipoprotein (apo)-AI. Triglyceride levels increased with alcohol, probably due to impaired fatty acid oxidation. Surprisingly, total cholesterol and LDL-C fell significantly, possibly due to altered pharmacokinetics, as reflected by the lower <i>t</i>_1/2. To assess the long-term clinical implications of these findings, a 6-week study into the effects of alcohol consumption on fluvastatin pharmacokinetics and lipid-lowering capacity was concluded in 26 patients with primary hypercholesterolemia (LDL-C 4.2 mmol/liter after dietary baseline period). Patients were randomized to 6-week treatment with 40 mg/day of fluvastatin, combined with either 20 g of alcohol diluted to 20% with lemonade, or with lemonade alone (reference). After a 6-week washout period, the 2 groups crossed over for a second 6-week treatment period. Measurements were made at the end of each treatment period. In the 20 patients who completed the study, no serious adverse events occurred. Alcohol did have some effect on fluvastatin pharmacokinetic parameters; a tendency to lengthen <i>t</i>_1/2 and to increase AUC and <i>t</i>_max compared with reference, without a difference in <i>C</i>_max between reference and alcohol. However, these pharmacokinetic effects did not correlate with differences in lipid parameters. Neither reference nor alcohol showed significant changes in HDL-C or triglyceride levels, but significant decreases in total cholesterol, LDL-C, and apo B were observed; these decreases did not differ significantly between reference and alcohol. In conclusion, alcohol consumption has no effect on the efficacy and safety of fluvastatin treatment in patients with primary hypercholesterolemia.

Effects of alcohol consumption on pharmacokinetics, efficacy, and safety of fluvastatin

Alcohol consumption is known to have beneficial effects on cardiac mortality, probably by increasing high density lipoprotein cholesterol (HDL-C). Alcohol also increases triglycerides and, in some studies, total cholesterol and low density lipoprotein cholesterol (LDL-C). Nothing is known, however, of the effects of alcohol on the pharmacokinetics and efficacy of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors. Consequently, 2 studies have been carried out to determine the effects of alcohol consumption on the pharmacokinetics and efficacy of the HMG-CoA reductase inhibitor fluvastatin. Firstly, the effects of acute alcohol consumption on a single, oral 40 mg dose of fluvastatin were examined in a reference-controlled, randomized, crossover study in 10 healthy volunteers. Measurements were made after ingestion of 70 g of ethanol diluted to 20% with lemonade and, following a 7-day period, after ingestion of lemonade alone (reference). The half-life ( t 1/2) of a single dose of fluvastatin was significantly reduced by acute alcohol consumption compared with reference, whereas the area under the time—concentration curve (AUC), peak concentration ( C max), and time to peak concentration ( t max) did not differ from the reference group. The lipid profile, measured 8 hr after administration, did not differ significantly from baseline in the reference group, apart from a slight reduction in apolipoprotein (apo)-AI. Triglyceride levels increased with alcohol, probably due to impaired fatty acid oxidation. Surprisingly, total cholesterol and LDL-C fell significantly, possibly due to altered pharmacokinetics, as reflected by the lower t 1/2. To assess the long-term clinical implications of these findings, a 6-week study into the effects of alcohol consumption on fluvastatin pharmacokinetics and lipid-lowering capacity was concluded in 26 patients with primary hypercholesterolemia (LDL-C 4.2 mmol/liter after dietary baseline period). Patients were randomized to 6-week treatment with 40 mg/day of fluvastatin, combined with either 20 g of alcohol diluted to 20% with lemonade, or with lemonade alone (reference). After a 6-week washout period, the 2 groups crossed over for a second 6-week treatment period. Measurements were made at the end of each treatment period. In the 20 patients who completed the study, no serious adverse events occurred. Alcohol did have some effect on fluvastatin pharmacokinetic parameters; a tendency to lengthen t 1/2 and to increase AUC and t max compared with reference, without a difference in C max between reference and alcohol. However, these pharmacokinetic effects did not correlate with differences in lipid parameters. Neither reference nor alcohol showed significant changes in HDL-C or triglyceride levels, but significant decreases in total cholesterol, LDL-C, and apo B were observed; these decreases did not differ significantly between reference and alcohol. In conclusion, alcohol consumption has no effect on the efficacy and safety of fluvastatin treatment in patients with primary hypercholesterolemia.

Effects of acute alcohol consumption on the pharmacokinetics and lipid-lowering capacity of fluvastatin

Effects of acute alcohol consumption on the pharmacokinetics and lipid-lowering capacity of fluvastatin

Effect of acute alcohol consumption on lithium kinetics

Lithium carbonate is used in several psychiatric disorders in the context of alcohol abuse. In a randomized, double-blind, crossover study the single-dose kinetics of lithium were followed after alcohol or placebo. Lithium carbonate capsules were taken by mouth by 10 healthy young men with alcohol on one occasion and with placebo on a separate occasion (at least 7 days apart). Lithium concentrations were determined in serum and urine samples for 24 hours after dosing and served as the basis for kinetic analysis. Acute alcohol had no effect on lithium absorption, elimination, distribution, or clearance. Alcohol did, however, increase the peak serum lithium level in nine of 10 subjects, from a mean of 0.62 mEq/L in the placebo condition to 0.70 mEq/L in the alcohol condition. Our data suggest that alcohol has limited effects on lithium carbonate kinetics. The possibility of elevated serum lithium concentrations when lithium is taken with alcohol is suggested.

PRESSOR EFFECTS OF ALCOHOL IN NORMOTENSIVE AND HYPERTENSIVE SUBJECTS

The effects of acute alcohol consumption and abstinence on blood pressure were studied in normal healthy subjects and in non-drinking and regularly drinking hypertensive patients. All subjects drank alcohol (1 g/kg body weight daily) for 5 days then abstained for 5 days. There was no significant difference in blood pressure in normal subjects during and after alcohol ingestion. However, in hypertensive non-drinkers both systolic and diastolic pressures when standing were significantly higher during the period of alcohol intake; supine blood pressure was not significantly higher. In hypertensive patients who drank regularly, standing and supine systolic and diastolic blood pressures were significantly higher during the period of drinking.

Effects of alcohol on the speech of alcoholics.

Speech disfluency resulting from alcohol intoxication was investigated in an experiment using established measures of nonfluency. Male alcoholic subjects (N = 16) read a standardized passage into a...