Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Alcoholics”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed2003

Women and alcohol susceptibility: could differences in alcohol metabolism predispose women to alcohol-related diseases?

These present studies have identified some important differences between male and female subjects in ethanol pharmacokinetics. The development of alcohol misuse in female subjects clearly altered the rate of ethanol elimination as well as increasing the circulating levels of blood acetaldehyde. The identification of an increased level of acetaldehyde in subjects homogenous for ADH(3)(2) genotype, may in part contribute to the higher incidence of alcohol-related damage, i.e. liver cirrhosis, associated with this ADH(3) genotype. The enhanced presystemic alcohol metabolism identified in female Caucasian controls, but not female alcohol misusers, may be an important factor in removing a significant quantity of ethanol during its first pass through the liver and thereby reduce circulating acetaldehyde concentrations.

Acetaldehyde↗
PubMed1986

Nosology and diagnosis of alcoholism. Issues and perspectives in subtyping (DSM III) simple alcoholism and alcoholism associated with other psychopathologies.

The presence of psychopathological syndromes in alcoholic in-patients was assessed using the NIMH-Diagnosis. The most stricking finding of this study was the high percentage of additional psychopathological syndromes associated to alcoholism. Based on this finding, a tentative classification of alcoholism is proposed. The urgent need for a comprehensive diagnostic scheme for alcoholism is underlined.

Alcoholism↗
PubMed1994

Purification of acetaldehyde dehydrogenase and alcohol dehydrogenases from Thermoanaerobacter ethanolicus 39E and characterization of the secondary-alcohol dehydrogenase (2 degrees Adh) as a bifunctional alcohol dehydrogenase--acetyl-CoA reductive thioesterase.

The purification and characterization of three enzymes involved in ethanol formation from acetyl-CoA in Thermoanaerobacter ethanolicus 39E (formerly Clostridium thermohydrosulfuricum 39E) is described. The secondary-alcohol dehydrogenase (2 degrees Adh) was determined to be a homotetramer of 40 kDa subunits (SDS/PAGE) with a molecular mass of 160 kDa. The 2 degrees Adh had a lower catalytic efficiency for the oxidation of 1 degree alcohols, including ethanol, than for the oxidation of secondary (2 degrees) alcohols or the reduction of ketones or aldehydes. This enzyme possesses a significant acetyl-CoA reductive thioesterase activity as determined by NADPH oxidation, thiol formation and ethanol production. The primary-alcohol dehydrogenase (1 degree Adh) was determined to be a homotetramer of 41.5 kDa (SDS/PAGE) subunits with a molecular mass of 170 kDa. The 1 degree Adh used both NAD(H) and NADP(H) and displayed higher catalytic efficiencies for NADP(+)-dependent ethanol oxidation and NADH-dependent acetaldehyde (identical to ethanal) reduction than for NADPH-dependent acetaldehyde reduction or NAD(+)-dependent ethanol oxidation. The NAD(H)-linked acetaldehyde dehydrogenase was a homotetramer (360 kDa) of identical subunits (100 kDa) that readily catalysed thioester cleavage and condensation. The 1 degree Adh was expressed at 5-20% of the level of the 2 degrees Adh throughout the growth cycle on glucose. The results suggest that the 2 degrees Adh primarily functions in ethanol production from acetyl-CoA and acetaldehyde, whereas the 1 degree Adh functions in ethanol consumption for nicotinamide-cofactor recycling.

Acetyl Coenzyme A↗
PubMedDate not supplied

ESBRA-Nordmann 1998 Award Lecture: Visual P3 as a potential vulnerability marker of alcoholism: evidence from the Amsterdam study of children of alcoholics. European Society for Biomedical Research on Alcoholism.

Recent data from the Amsterdam Study of Children of Alcoholics add to the evidence for considering the P300 or P3 component of the event-related potential (ERP) as a potential vulnerability marker of alcoholism. In this study, multi-channel ERPs were recorded from 7- to 18-year-old children of alcoholics (COAs) and age- and sex-matched low-risk controls using several experimental paradigms, including a visual novelty oddball task and a visual selective attention task. The results indicated that differences between COAs and controls in the visual P3 amplitude: (1) can be elicited both actively by task-relevant target stimuli and passively by irrelevant novel stimuli; (2) are a function of both the attentional relevance and the target properties of the eliciting stimulus; (3) are mediated by multiple brain generators, rather than by a single generator; (4) originate from a difference in the strength, rather than in the spatial configuration, of the underlying brain generators; (5) cannot be accounted for by differences in visual attention-related earlier occurring ERP components; and (6) can be moderated by current behavioural and emotional problems, general intellectual ability, and socio-economic background. These findings support the notion that a relatively small visual P3 amplitude in COAs reflects heritable biases in attention and information processing that are related to their increased vulnerability to alcoholism.

Adolescent↗
PubMed2003

Confirmation of alcohol preference quantitative trait loci in the replicate high alcohol drinking and low alcohol drinking rat lines.

OBJECTIVE: Selective breeding has been employed to develop replicate high-alcohol-drinking (HAD1 and HAD2) and low-alcohol-drinking (LAD1 and LAD2) rat lines from the heterogeneous N/Nih rat. Within-family selection and a rotational breeding design were used to discourage inbreeding (Li et al., 1993). A genome screen was previously performed using 459 HAD1xLAD1 F2 progeny to identify quantitative trait loci (QTLs) on rat chromosomes 5, 10, 12 and 16 that contribute to alcohol preference and consumption in these non-inbred rat models of alcoholism. METHODS: To confirm these QTLs in the replicate lines, 16 HAD2 and 16 LAD2 rats were genotyped for microsatellite markers within each of these QTL intervals. RESULTS: Review of the genotypic data support confirmation of the QTLs on chromosomes 5 and 10; several markers in the QTL region display different alleles in the HAD2 and LAD2 rats, suggesting linkage disequilibrium between the microsatellite markers and the QTL. Although the QTL on chromosome 12 had the highest LOD score in the HAD1 and LAD1 studies, little evidence supported confirmation of this QTL based on the genotyped markers. CONCLUSIONS: Further evaluation of each of these QTL regions is ongoing in a sample of HAD2xLAD2 F2 progeny currently being generated that will be used to assess the evidence of linkage in each of these QTL regions.

Alcohol Drinking↗
PubMed1995

Medicolegal alcohol determination: variability of the blood- to breath-alcohol ratio and its effect on reported breath-alcohol concentrations.

There is substantial agreement among scientists that the variability of a person's blood- to breath-alcohol ratio contributes significantly to the experimental error in results from breath-alcohol analysis. Some have argued that the need to correct for this source of error can be eliminated by reporting breath test results in units of breath-alcohol concentration rather than blood-alcohol concentration. A simple mathematical proof is presented to demonstrate that this is not the case. Moreover, the scientific and legal flaws of this argument are discussed, and recommendations are offered for dealing with the problems that have developed from adoption of this view.

Alcoholism↗
PubMed2001

Local cerebral glucose utilization rates in alcohol-naïve high-alcohol-drinking (HAD) and low-alcohol-drinking (LAD) rats.

BACKGROUND: The present study compared baseline local cerebral glucose utilization (LCGU) values within reward-relevant brain regions in alcohol-naïve, adult male high-alcohol-drinking (HAD) and low-alcohol-drinking (LAD) rats from replicate lines 1 and 2. METHODS: 2-[14C]Deoxyglucose ([14C]2-DG) was injected (125 microCi/kg) intravenously during the rats' dark cycle. Timed arterial blood samples were collected over 45 min and assayed for glucose as well as [14C]2-DG content. Rats were then decapitated; their brains quickly removed and frozen in isopentane at -50 degrees C. Coronal sections from each brain were apposed to film and exposed for 2 days. Image densities were analyzed using quantitative autoradiography. RESULTS: Data were collected from several key limbic (nucleus accumbens, ventral tegmental area, olfactory tubercle, amygdala, hippocampus, ventral pallidum, and septum), basal ganglia, cortical (medial prefrontal, frontal, parietal, temporal, occipital, entorhinal, pyriform, and cingulate), and subcortical (thalamus, habenula, and superior colliculus) structures. Because there were no significant differences between the replicates within each drinking line, data from the two replicates were combined to determine drinking line differences. When both replicate lines were combined, there were trends toward higher (approximately 15%) LCGU rates in HAD (n = 15) versus LAD (n = 16) rats within the parietal and occipital cortices, but neither of these line differences reached statistical significance (p < 0.01). CONCLUSIONS: The findings suggested that, within the HAD and LAD replicate rat lines, the selection for alcohol preference did not lead to differences in functional brain activity, as measured with the 2-DG method.

Alcohol Drinking↗
PubMed1983

The role of alcohol availability in alcohol consumption and alcohol problems.

The major theoretical approaches that have provided competing explanations for the distribution and nature of alcohol problems are reviewed and assessed. The sociocultural model and studies are briefly discussed with major emphasis given to the particular studies that have focused on different conceptions and dimensions of availability. Attempts to integrate the sociocultural model and the distribution of consumption model are also reviewed. A recent integrated model finds specific relationships between physical availability or the different types of outlets, with social area characteristics of different populations, and some four different alcohol problems, including cirrhosis, public drunk arrests, and misdemeanor and felony drunk driving arrests. Specific social area characteristics representing social class, minority status, and other structural features such as unemployment and women's labor force participation become implicated in alcohol problems independently of the effects of differing levels of availability. Additional related research on licensing and enforcement practices, beliefs, and attitudes of ABC personnel are also reviewed in relation to the general issue of availability. Other recent research on social and psychological dimensions of availability are also reviewed. Cross-sectional time series modeling is suggested as a technique for determining causal processes.

Alcohol Drinking↗
PubMed1985

Role of alcohol dehydrogenase in the swift increase in alcohol metabolism (SIAM). Studies with deer mice deficient in alcohol dehydrogenase.

Previous studies have shown that rates of ethanol metabolism increase markedly 2-4 hr after the administration of ethanol in rats and in four inbred strains of mice. This phenomenon, called the swift increase in alcohol metabolism (SIAM), also exists in humans. To determine whether alcohol dehydrogenase (ADH) is necessary for the SIAM response, we compared ethanol metabolism in two strains of the deer mouse, Peromyscus maniculatus. One strain lacks alcohol dehydrogenase (ADH-negative), whereas the other strain has normal ADH levels (ADH-positive). Rates of ethanol elimination were determined after a single intraperitoneal injection of ethanol at different doses (0.5 to 3.0 g/kg) and also after both strains were exposed to various levels of ethanol vapor for 4 hr. The ADH-positive strain exhibited up to a 72% increase in the rate of ethanol elimination after exposure to ethanol vapor compared to the ethanol-injected controls. In contrast, treatment with ethanol vapor did not alter rates of ethanol elimination in the ADH-negative strain. These data demonstrate clearly that ADH is required for SIAM in the deer mouse. In addition, in both the ADH-positive and the ADH-negative strain, rates of ethanol elimination increased in both the ethanol-injected and vapor-treated groups 2- to 3-fold as the dose of ethanol was increased from 100 to 500 mg/100 ml. Thus, it is concluded that this "concentration effect" of ethanol on rates of ethanol metabolism does not involve ADH in the . deer mouse.

Alcohol Dehydrogenase↗
PubMed2004

Comparison of new alcohol use test, the Helsinki Alcohol Use Test questionnaire, and Alcohol Use Disorders Identification Test and laboratory markers serum gamma-glutamyl transferase and carbohydrate-deficient transferrin.

The purpose of the present study was to compare and evaluate the new Helsinki Alcohol Use Test (HAUT) and Alcohol Use Disorders Identification Test (AUDIT) as screening instrument in the general working population. The relationship between the HAUT and serum gamma-glutamyl transferase (GGT), and carbohydrate-deficient transferrin (CDT) was also evaluated. Our results seem to indicate that the HAUT has good performance as screening instrument for alcohol-related problems in the general population.

Alcohol Drinking↗
PubMed1998

Contribution to first-pass metabolism of ethanol and inhibition by ethanol for retinol oxidation in human alcohol dehydrogenase family--implications for etiology of fetal alcohol syndrome and alcohol-related diseases.

The alcohol dehydrogenase (ADH) family is involved in the metabolism of both ethanol and retinoids. To quantitatively assess the potential contributions to first-pass metabolism of ethanol and the ethanol interference with retinoid homeostasis, saturation kinetics for ethanol oxidation as well as inhibition kinetics by ethanol for all-trans-retinol oxidation of human class I alpha alpha, beta1beta1, beta2beta2, gamma1gamma1, class II pi pi, class III chi chi, and class IV mu mu were evaluated and compared. Class I and class II ADHs exhibited substrate inhibition with inhibition constants ranging over 250-720 mM (except gamma1gamma1) ethanol. Class IV ADH displayed no appreciable inhibition up to 1 M ethanol. Activity of the class III enzyme (190 nM subunit) was undetectable at 250 mM ethanol. The kinetic simulations indicate that the hepatic pi pi and the gastric mu mu can most effectively contribute to first-pass metabolism of alcohol. The Michaelis constant (Km), turnover number (k(cat)), and catalytic efficiency (k(cat)/Km) for retinol oxidation relative to that for ethanol oxidation in class I, class II, and class IV ADHs ranged over 0.00022-1.3, 0.071-0.48, and 0.24-650, respectively. Ethanol was a competitive inhibitor against retinol for class I, II, and IV ADHs with apparent inhibition constants ranging over 0.037-11 mM, indicating that retinoic acid synthesis through the ADH pathways can be tremendously blocked during social/heavy drinking. These findings support the notion that first-pass metabolism of alcohol may occur mainly in the liver through class II pi pi and that cellular retinoid signaling may be perturbed by ethanol via ADH pathways.

Alcohol Dehydrogenase↗
PubMed1990

Genotyping study of alcohol dehydrogenase class I polymorphism in French patients with alcoholic cirrhosis. The French Group for Research on Alcohol and Liver.

Comparison of alcohol dehydrogenase polymorphism at the loci ADH2 and ADH3 is made in France between 46 alcoholic cirrhotic patients and 39 controls, by genotyping technique using polymerase chain reaction on blood microsample collected on blotting paper. The genotype distributions are similar, with low frequency of the ADH2(2) allele. Polymorphism at the ADH3 locus is not a genetic factor for alcoholic cirrhosis in France.

Adult↗
PubMed2005

Magnetic resonance imaging findings in substance abuse: alcohol and alcoholism and syndromes associated with alcohol abuse.

Alcohol abuse is common among the population and results in significant diseases that shorten life span. Ethanol may result in chronic brain changes such as atrophy but may also result in neurologic disease that may be acute or chronic and sometimes life threatening. Accompanying vitamin deficiencies may lead to Wernicke's encephalopathy and changes in serum osmosis may lead to several acute demyelinating disorders. In addition, pregnant women who consume alcohol place their babies at high risk for the fetal alcohol syndrome. In this article we review these disorders and emphasize their imaging features.

Alcohol-Induced Disorders, Nervous System↗
PubMed1989

Alcoholic and non-alcoholic liver disease in relation to alcohol consumption in Scotland, 1978-84. Part I: Epidemiology of liver diseases.

A common strategy in epidemiological studies linking alcohol consumption in the general population with liver cirrhosis mortality is to use non-specific cirrhosis mortality rates in which alcoholic and non-alcoholic causes of death are not distinguished. Evidence is presented from Scottish mortality data for 1979 to 1984 that the two forms of cirrhosis have quite different epidemiological profiles. Similar findings emerge from morbidity data. The two forms of disease should be distinguished in future studies in which liver cirrhosis is used as a proxy for consumption, despite the manifest shortcomings of currently available data.

Adult↗
PubMed1994

Synaptic membrane responses to acute and chronic alcohol intoxication in high alcohol sensitive (HAS) and low alcohol sensitive (LAS) selectively bred rats.

HAS (high alcohol sensitive) and LAS (low alcohol sensitive) lines of rats have been selectively bred based on their differences in ethanol-induced sleep time. In the present study, the two lines were compared to examine another central effect of acute alcohol intoxication: namely, hypothermia. As the disturbances in membrane microorganization have been associated with the nervous system's sensitivity and tolerance to ethanol, the synaptic plasma membrane fluidity and acute sensitivity to ethanol were also evaluated by fluorescence polarization of DPH probes in the HAS and LAS rats. The two lines did not differ in the magnitude of their hypothermic response after acute injection of ethanol (3 g/kg body wt, i.p.). Although membranes in the HAS line were slightly more rigid than in the LAS line, the level of membrane disordering after acute ethanol addition was identical for the two lines in the region examined with the DPH probe. Following the chronic intoxication of the rats, the two lines developed tolerance to the hypnotic and hypothermic effects of ethanol. In the same way, a membrane resistance (i.e. tolerance) to the disordering effect of acute ethanol addition developed in the region probed with DPH. In general, the LAS line showed a more pronounced level of tolerance than the HAS line at both the functional and membrane level. These results suggest that different measures used to assess the depressant action of ethanol, such as sleep time, hypothermia or membrane disordering, may not be related and could indicate different genetic origins.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholic Intoxication↗
PubMed1982

Alcohol availability, alcoholic beverage sales and alcohol-related problems.

A theoretical integration and an empirical test of the sociocultural model and the distribution of consumption model of alcohol problems is made for 51 California counties. In the counties of California, the kinds and number of outlets of alcoholic beverages are differentially related to the social area characteristics and to arrest rates for public drunkenness, misdemeanor and felony drunken-driving arrest rates and cirrhosis mortality rates.

Alcohol Drinking↗
PubMed1973

Microbial metabolism of amino alcohols. Metabolism of ethanolamine and 1-aminopropan-2-ol in species of Erwinia and the roles of amino alcohol kinase and amino alcohol o-phosphate phospho-lyase in aldehyde formation.

1. Growth of Erwinia carotovora N.C.P.P.B. 1280 on media containing 1-aminopropan-2-ol compounds or ethanolamine as the sole N source resulted in the excretion of propionaldehyde or acetaldehyde respectively. The inclusion of (NH(4))(2)SO(4) in media prevented aldehyde formation. 2. Growth, microrespirometric and enzymic evidence implicated amino alcohol O-phosphates as aldehyde precursors. An inducibly formed ATP-amino alcohol phosphotransferase was partially purified and found to be markedly stimulated by ADP, unaffected by NH(4) (+) ions and more active with ethanolamine than with 1-aminopropan-2-ol compounds. Amino alcohol O-phosphates were deaminated by an inducible phospho-lyase to give the corresponding aldehydes. This enzyme, separated from the kinase during purification, was more active with ethanolamine O-phosphate than with 1-aminopropan-2-ol O-phosphates. Activity of the phospho-lyase was unaffected by a number of possible effectors, including NH(4) (+) ions, but its formation was repressed by the addition of (NH(4))(2)SO(4) to growth media. 3. E. carotovora was unable to grow with ethanolamine or 1-aminopropan-2-ol compounds as sources of C, the production of aldehydes during utilization as N sources being attributable to the inability of the microbe to synthesize aldehyde dehydrogenase. 4. Of seven additional strains of Erwinia examined similar results were obtained only with Erwinia ananas (N.C.P.P.B. 441) and Erwinia milletiae (N.C.P.P.B. 955).

Acetaldehyde↗
PubMed2006

The alcohol-preferring AA and alcohol-avoiding ANA rats: neurobiology of the regulation of alcohol drinking.

The AA (alko, alcohol) and ANA (alko, non-alcohol) rat lines were among the earliest rodent lines produced by bidirectional selection for ethanol preference. The purpose of this review is to highlight the strategies for understanding the neurobiological factors underlying differential alcohol-drinking behavior in these lines. Most early work evaluated functioning of the major neurotransmitter systems implicated in drug reward in the lines. No consistent line differences were found in the dopaminergic system either under baseline conditions or after ethanol challenges. However, increased opioidergic tone in the ventral striatum and a deficiency in endocannabinoid signaling in the prefrontal cortex of AA rats may comprise mechanisms leading to increased ethanol consumption. Because complex behaviors, such as ethanol drinking, are not likely to be controlled by single factors, system-oriented molecular-profiling strategies have been used recently. Microarray based expression analysis of AA and ANA brains and novel data-mining strategies provide a system biological view that allows us to formulate a hypothesis on the mechanism underlying selection for ethanol preference. Two main factors appear active in the selection: a recruitment of signal transduction networks, including mitogen-activated protein kinases and calcium pathways and involving transcription factors such as Creb, Myc and Max, to mediate ethanol reinforcement and plasticity. The second factor acts on the mitochondrion and most likely provides metabolic flexibility for alternative substrate utilization in the presence of low amounts of ethanol.

Alcohol Drinking↗