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PubMed1990

[MR tomography and computer tomography of alcohol-induced brain tissue changes].

Results of MRI in five alcoholics suffering from acute neurologic disorders such as ataxia, ophthalmoplegia and confusion are presented. The detection of focal cerebral lesions of high signal intensity in T2-weighted Spin-Echo- and Gradient-Echo-images in periventricular white matter, thalamus and pons combined with patients history and clinical presentation led to the diagnosis of Wernicke-Encephalopathia and Pontine Myelinolysis. MRI was far more sensitive compared with CT.

Adult↗
PubMed1990

Effects of chronic alcoholism on hemispheric functioning: an examination of gender differences for cognitive and dichotic listening tasks.

A pattern of intact verbal abilities and impaired visuospatial abilities has led to a hypothesis of alcohol-induced right-hemisphere dysfunction in male chronic alcoholics. The applicability of this hypothesis to chronic female alcoholics was examined by administering the WAIS-R, Stark Paired Associates Tasks, and dichotic listening tasks to 15 male and 10 female alcoholics and 15 male and 10 female controls of similar age and education. Alcoholics had significantly lower Full Scale IQ scores on the WAIS-R but neither sex had a Verbal-Performance IQ difference indicative of right-hemisphere dysfunction. Male alcoholics showed deficits on both the Verbal and Visuospatial Stark Tasks, the deficit being greater on the Visuospatial Task. Male alcoholics showed an increased right-ear superiority on the verbal dichotic listening task and a decreased left-ear superiority on the musical dichotic listening task, both indicative of right-hemisphere dysfunction. The results, except for the WAIS-R, support the hypothesis that male but not female chronic alcoholics exhibit right-hemisphere dysfunction. Females, alcoholic or not, appear to be less lateralized in function.

Adult↗
PubMed1989

Alcohol use and retinal vessels: insights into the mechanism of alcohol-induced stroke.

Alcohol use is a recognized risk factor for stroke. We hypothesized that alcohol use may increase the risk of stroke, independent of an effect on blood pressure, by causing cerebral vasoconstriction. To examine this, we used retinal vessels as a marker for cerebral vessels and analysed the cross-sectional associations between alcohol use and total retinal vessel width in 741 Japanese and 434 American white male telephone executives. Systolic and diastolic blood pressures were negatively associated with retinal vessel width in the Japanese (p less than 0.0001, 0.0001, respectively) but this association did not achieve statistical significance in the Americans (p less than 0.1, 0.3). Japanese drinkers had a larger mean retinal vessel width than Japanese abstainers, while American drinkers had a smaller retinal vessel width than abstainers. These associations between alcohol use and retinal vessel width were not significant within nationalities but the interaction between alcohol use and nationality was significant, independent of other stroke risk factors (p less than 0.04). Although these results do not support the initial hypothesis, they are consistent with known biological differences in alcohol metabolism between Japanese and American men and support different effects of alcohol use on retinal vessel calibre in these two nationalities.

Adult↗
PubMed1992

Role of alcohol abuse in nutritional immunosuppression.

Nutritional status is an important determinant of the host resistance against infections and tumors. Alcohol interferes in various ways with the complex system of nutritional immunomodulation. Alcohol acts directly on mechanical barriers in the gastrointestinal tract and increases permeability of intestinal walls, which results in a reduced exclusion of immunogenic material in the intestine. Alcohol further affects granulocytopoiesis and suppresses various immune functions. Indirect effects on the immune response are caused by alcohol-induced malnutrition. Heavy alcohol abuse is associated with a high energy intake derived by alcohol and an inadequate intake of protein, vitamins and minerals. In addition, alcohol abuse impairs absorption, utilization, storage and excretion of nutrients, which together with inadequate nutrient intakes results in nutritional immunosuppression. The high incidence of infections in alcoholics could be one consequence of the alcohol-induced immunosuppression.

Alcoholism↗
PubMed1990

The effect of alcohol consumption on recency discrimination ability: an early screening test for alcohol-induced cognitive impairment.

In this short study the relationship between recency discrimination ability and a measure of alcohol intake was examined using a series of regression analyses. Semi-partial correlations were extracted in order to evaluate which variables (level of alcohol consumption, age and IQ) best predicted recency discrimination performance on both verbal and non-verbal tasks. Results showed that while IQ best predicted performance on the verbal task both IQ and alcohol intake were significant predictors on the non-verbal task. The results are discussed in relation to current findings and the continuity hypothesis.

Adult↗
PubMed1987

Alcohol-induced changes in pituitary-adrenal activity during pregnancy.

This study examined the interactive effects of ethanol and nutritional status on pituitary-adrenal function of pregnant females consuming high doses of ethanol throughout gestation. Three liquid diets were formulated ranging in protein content from suboptimal to supraoptimal (18%, 25%, or 32% of total calories) in terms of pregnancy requirements, while ethanol was held constant at high levels (36% of total calories). In addition to the alcohol group (A), both pair-fed (PF) and ad libitum-fed control (C) groups were included in each diet regimen. Basal levels of corticosterone and the adrenocortical response to stress were measured in dams on days 11, 16, or 21 of gestation. Plasma levels of corticosterone-binding globulin (CBG) were also measured on gestation days 16 and 21. Maternal adrenal weights, basal corticosterone levels, the adrenocortical response to stress, and the corticoid stress increment were all significantly increased in A compared to both PF and C females. Plasma CBG levels of A females were similar to or less than those of PF and C females. Thus alcohol consumption significantly increased maternal pituitary-adrenal activity as early as day 11 of gestation and these effects on hormonal function increased as gestation progressed. This adrenocortical hyperactivity was relatively unaffected by maternal nutritional status and thus appears specific to alcohol.

Alcoholism↗
PubMed1990

New approaches to research on the long-term consequences of prenatal exposure to alcohol.

As the summary presentation of a symposium on prenatal alcohol-induced brain damage and long-term postnatal consequences, this paper proposes the establishment of two main research priorities--to begin to correlate long-term behavioral effects with alterations in underlying neural substrates, and to explore the mechanisms of neuroteratogenicity. To reach these goals, three objectives are described. First, animal and human research must become more interrelated. Second, experimental observations should be integrated into formal models that incorporate both neural structure and function. Third, researchers should choose well-defined dependent measures that are derived from models of brain function based on modern concepts of cognitive neuroscience. Examples of neuropsychological tests that may serve as the bases for structure/function relationships are presented. Incorporating these objectives into future research will facilitate understanding of the fundamental issues concerning prenatal alcohol exposure and will begin to provide the bases for rational intervention or treatment.

Alcohol Drinking↗
PubMed1990

Cell population depletion associated with fetal alcohol brain damage: mechanisms of BAC-dependent cell loss.

Neuronal death is one of the most serious consequences of alcohol exposure during development. Studies described in this paper used a neonatal rat model to address factors affecting neuronal death following alcohol exposure during the period of rapid brain growth, and relate them to possible mechanisms of damage. The profile of blood alcohol concentrations (BACs) is an important variable influencing both brain growth deficits and neuronal death--a smaller daily dose of alcohol can be more damaging than a larger daily dose, if it is consumed in a binge-like pattern that produces relatively higher BACs. Alcohol exposure for a single day also can be damaging, producing both brain growth deficits and neuron loss, if high BACs are obtained. Various brain regions and different neuronal populations within a given brain area exhibit different degrees of vulnerability. Some neuronal loss clearly is a function of cell death due to direct effects of alcohol, while other deficits may be due to either primary or secondary effects of the alcohol insult. In the cerebellum, a maturational or metabolic factor also appears to be involved with alcohol-induced neuronal death. Immunocytochemical studies using a monoclonal antibody against microtubule-associated protein 2 (MAP2) indicated that cerebellar lobules containing Purkinje cells that are in the process of extending dendrites are ones that are more vulnerable to alcohol than lobules containing Purkinje cells that mature later. Alcohol exposure during brain development may be producing neuron attrition in multiple ways, including disruption of membrane integrity, inhibition of protein synthesis or other alterations such as lipid solubility, or by disruption of cytoskeletal elements.

Animals↗
PubMed1987

Use of enzymes for the diagnosis of alcohol-related organ damage.

Elevated levels of serum enzymes are frequently associated not only with alcohol-related organ damage but also with excessive alcohol consumption and alcoholism without significant tissue injury. However, both in the early detection of alcoholism as well as also in the diagnosis of alcohol-related diseases the sensitivities and specificities of these enzyme markers vary considerably. They may be influenced by nonalcohol-related diseases, enzyme-inducing drugs, nutritional factors, metabolic disorders, age, smoking, etc. Consequently, we have neither a single laboratory test--enzyme marker--nor a test combination that is reliable enough for the exact diagnosis between alcohol- and nonalcohol-related organ damage. In most cases it is possible to determine the tissue from which the elevated enzyme is derived, but only occasionally enzyme changes reflect the quantity of the tissue injury. Gamma-glutamyltransferase (GGT) is the most widely used laboratory marker of alcoholism and heavy drinking, detecting 34-85% of problem drinkers and alcoholics. However, the unspecificity of increased serum GGT limits its use for general screening purposes. Its value in the follow-up of various treatment programs, however, is well established. An elevated level of serum aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) in an alcoholic or a heavy consumer indicates alcohol-induced organ damage. The use of test combinations significantly improves the information received with single serum enzyme determinations. An ASAT/ALAT ratio greater than 1.5 can be considered as highly suggestive for the alcoholic etiology of the liver injury. Still better discrimination between alcoholic and nonalcoholic origin of the liver disease may be achieved by the determination of the ratio of GGT to alkaline phosphatase. If this ratio exceeds 1.4 the specificity of the finding in favor for alcoholic liver injury is 78%. The determination of the mitochondrial isoenzyme of ASAT also improves the diagnostic value of ASAT determination. The ratio of mitochondrial isoenzyme to total over 4 is highly suggestive for alcohol-related liver injury. In general, however, the determination of serum activities of other enzymes such as ornithine carbamyl transferase, lactate dehydrogenase, isocitrate dehydrogenase, sorbitol dehydrogenase, alcohol dehydrogenase, guanase, aldolase, alkaline phosphatase or glutathione S-transferase do not significantly improve the diagnostic information obtained with more conventional laboratory markers of liver injury.(ABSTRACT TRUNCATED AT 400 WORDS)

Alanine Transaminase↗
PubMed1988

Experience-dependent cognitive recovery in alcoholics: a task component strategy.

Visuospatial problem-solving deficits following chronic alcohol abuse may not readily recover spontaneously after drinking cessation but may reverse with appropriate environmental stimulation. To determine if such recovery in alcoholics under age 40 may be accelerated by training with components of an initially impaired task (Trails B), this study employed four groups of alcoholics (N = 53) and a group of matched controls (N = 13). Two alcoholic groups received two consecutive cognitive remediation sessions during the latter 2 weeks of a 1-month treatment program, and two groups of alcoholics received no remediation. Results confirmed that recovery of visuospatial problem-solving skills is facilitated by training with task components (experience-dependent recovery) while spontaneous recovery during the first month of abstinence is minimal for this task. These findings demonstrate the efficacy of cognitive remediation in reversing some alcohol-induced cognitive impairment and have important implications for improving alcohol treatment outcome and adaptive functioning.

Adult↗
PubMed1991

Effect of drugs of abuse on psychiatric symptoms among hospitalized schizophrenics.

In a group of 71 inpatient schizophrenics with no other concurrent psychiatric diagnosis except for dependence on one drug, we ascertained the subjective effect their drug of abuse had on their psychiatric symptoms 2 weeks prior to hospitalization. Psychiatric symptoms were assessed by means of the Hopkins Symptom Checklist (Revised) (SCL-90R). Cocaine addicts, but not alcoholics, reported aggravation more often than improvement of symptoms. Alcoholics reported alcohol-induced symptom improvement with a similar frequency as alcohol-induced symptom aggravation.

Adult↗
PubMed1990

Teratogenic effects of alcohol on brain development.

There is convincing evidence that alcohol is teratogenic both in humans and animals and that its most devastating effects are on the developing brain. However, much information is still needed to determine the circumstances that increase the risk and severity of fetal alcohol-induced brain damage and to identify the mechanisms underlying such damage. Animal research has been used to address these issues because, for the most part, they are unapproachable experimentally in humans. In the past, the rather restricted focus of research into the teratology of alcohol has led to several theoretical biases. Recent findings conflict with these biases. Alcohol-induced damage to the developing brain encompasses a longer developmental time-frame, affects more cell populations, occurs at lower levels of exposure, produces greater numbers of permanent effects, and is modulated by more factors than was initially suggested by earlier teratological studies.

Abnormalities, Drug-Induced↗
PubMed2025

Differential Expression of Erythrocyte Proteins in Patients with Alcohol Use Disorder.

Alcohol Use Disorder (AUD) poses global health challenges, and causes hematological alterations such as macrocytosis and oxidative stress. Disruption of protein structures by alcohol and/or its metabolites may exacerbate AUDs; proteomics can elucidate the underlying biological mechanisms. This study examined the proteins differentially expressed in the cytosol and membrane fractions of erythrocytes obtained from 30 male patients with AUD, comparing them to samples from 15 age- and BMI-matched social drinkers (SDs) and 15 non-drinkers (control). The analysis aimed to identify the molecular differences related to alcohol consumption. The AUD patient subgrouping was based on mean corpuscular volume (MCV), with 16 individuals classified as having a normal MCV and 14 having a high MCV. Proteins were separated via two-dimensional(2D)-gel electrophoresis, digested with trypsin, and identified via Matrix-Assisted Laser Desorption/Ionization Time-of-Flight (TOF) mass spectrometry (MALDI-TOF/TOF). Additionally, levels of malondialdehyde and 4-hydroxyalkenals (MDA + HAE), reduced glutathione (GSH), oxidized glutathione (GSSG), serum carbohydrate-deficient transferrin (%CDT), disialotransferrin (%DST), and sialic acid (SA) were analyzed. The results showed increased MDA + HAE and decreased total thiols in AUD patients, with GSSG elevated and the GSH/GSSG ratio reduced in the AUD MCV-high subgroup. Serum %CDT, %DST, and SA were significantly higher in AUD. Compared to the control profiles, the AUD group exhibited differential protein expression. Few proteins, such as bisphosphoglycerate mutase, were downregulated in AUD versus control and SD, as well as in the MCV-high AUD subgroup. Conversely, endoplasmin and gelsolin were upregulated in AUD relative to control. Cytoskeletal proteins, including spectrin-alpha chain, actin cytoplasmic 2, were overexpressed in the AUD group and MCV-high AUD subgroup. Several proteins, such as 14-3-3 isoforms, alpha-synuclein, translation initiation factors, heat shock proteins, and others, were upregulated in the MCV-high AUD subgroup. Under-expressed proteins in this subgroup include band 3 anion transport protein, bisphosphoglycerate mutase, tropomyosin alpha-3 chain, uroporphyrinogen decarboxylase, and WD repeat-containing protein 1. Our findings highlight the specific changes in protein expression associated with oxidative stress, cytoskeletal alterations, and metabolic dysregulation, specifically in AUD patients with an elevated MCV. Understanding these mechanisms is crucial for developing targeted interventions and identifying biomarkers of alcohol-induced cellular damage. The complex interplay between oxidative stress, membrane composition, and cellular function illustrates how chronic alcohol exposure affects cellular physiology.

Humans↗
PubMedDate not supplied

Alcohol intoxication results in rapid loss in free magnesium in brain and disturbances in brain bioenergetics: relation to cerebrovasospasm, alcohol-induced strokes, and barbiturate anesthesia-induced deaths.

In vivo 31P-nuclear magnetic resonance (31P-NMR) spectroscopy and ion-selective electrode measurements were undertaken to determine if administration of acute doses of alcohol (ALC, 0.2-6.6 g/kg), and lethal doses of barbiturate anesthesia, exert any influence on: (1) brain cellular bioenergetics, intracellular free Mg ([Mg2+]i) and intracellular pH (pHi), and (2) serum levels of ionized Mg (IMg2+), ionized calcium (ICa2+) and K+. Approximately 20-30 min after intraperitoneal administration of ALC to anesthetized rats, brain phosphocreatine (PCr)/ATP and PCr/inorganic phosphate (P(i)) ratios dropped from 2.5 to 1.7 and from 6.6 to 2.2, respectively, P(i) rose 20-200% (depending upon ALC dose), and free ADP and creatine rose significantly. ALC induced rapid decreases in the cytosolic phosphorylation potential (CPP) and free energy of ATP hydrolysis (-delta G/delta E). Following ALC administration, brain [Mg2+]i dropped rapidly (within 4-30 min) and significantly; the greater the dose of ALC, the greater the loss in brain [Mg2+]. Correlations were found between [Mg2+]i, PCr/ATP, CPP and delta G/delta E after ALC but not in control brains. Rats that exhibited ALC-induced strokes and death (unlike barbiturate death) exhibited huge elevations in [Mg2+]i. Although ALC administration does not alter brain pHi at least (up to 70 min), ALC- and barbiturate-induced death produces rapid brain intracellular acidosis. Concomitant with ALC-induced alterations in [Mg2+]i and brain cellular bioenergetics, we noted that ALC administration results in rapid elevations in serum IMg2+ and K+ but not ICa2+. These results suggest that ALC administration and heavy or binge-drinking of ALC (1) can result in rapid alterations in brain bioenergetics, [Mg2+]i and pHi, and (2) result in rapid elevations in serum IMg2+ and K+ in rats. In addition, ALC- and barbiturate-induced deaths do not appear to produce identical alterations in brain bioenergetics and [Mg2+]i, and lastly binge or heavy drinking of ALC may result in stroke-like events and sudden death via rapid alterations in brain cellular bioenergetics.

Alcoholic Intoxication↗
PubMed1979

Alcohol-related diseases and carcinogenesis.

Possible mechanisms whereby alcohol abuse and alcohol-related diseases may promote the development of cancer are analyzed. The mechanisms discussed include: (a) contact-related local effects on the upper gastrointestinal tract; (b) the presence of low levels of carcinogens in alcoholic beverages; (c) induction of microsomal enzymes involved in carcinogen metabolism; (d) various types of cellular injury produced by ethanol and its metabolites and their relationship to cancer, particularly in the liver; (e) the nutritional disturbances frequently associated with alcohol abuse. The relationship between alcohol-induced cirrhosis and hepatocellular carcinoma is also discussed, and case histories of patients seen at the Bronx Veterans Administration Medical Center with hepatocellular carcinoma in the absence of cirrhosis are reviewed. Data are presented demonstrating the induction, by chronic ethanol consumption, of microsomal enzymes which convert procarcinogens to carcinogens. These data were derived from experiments in which the ability of microsomes isolated from liver, intestine, and lung tissues of ethanol-fed and control rats to activate several test carcinogens was examined in the Ames Salmonella-mutagenicity test. The hypothesis is presented that ethanol-mediated induction of enzyme systems which activate procarcinogens to carcinogens in various tissues contributes to the enhanced incidence of cancer in the alcoholic.

Alcoholism↗