2024-03-28T17:31:01Zhttp://open-archive.highwire.org/handler
oai:open-archive.highwire.org:alcalc:35/6/5372015-05-19HighWireOUPalcalc:35:6
PHARMACOTHERAPY OF ALCOHOLISM: GAPS IN KNOWLEDGE AND OPPORTUNITIES FOR RESEARCH
Kranzler, Henry R.
INVITED REVIEW
During the past decade, renewed interest in medications to prevent relapse in alcoholics has yielded a number of promising candidates. Although two of these medications, naltrexone and acamprosate, are currently in clinical use in a number of countries, overall, their effectiveness appears to be limited. Disulfiram, the deterrent medication that was approved 50 years ago for the treatment of alcoholism, has not consistently been shown to be efficacious. However, since inadequate dosing and other modifiable factors may limit its deterrent effects, the identification of a more potent metabolite of disulfiram appears to warrant further evaluation. Studies of serotonergic agonists for treatment of alcoholism have also yielded inconsistent results. There is evidence, however, that subgroups of alcoholics may respond well to such medications, suggesting that treatment matching may enhance their efficacy. In addition, nalmefene, a compound with effects similar to naltrexone, as well as a sustained release formulation of naltrexone, may enhance the beneficial effects of opioid antagonist therapy. Despite these developments, much remains to be learned about the pharmacotherapy of alcoholism. The ongoing development and evaluation of novel medications should be given a high priority. However, such basic issues as the optimal dosing strategy and duration of treatment for existing therapies are not known. Similarly, combination therapy, involving either multiple medications or the combination of medication with specific psychotherapies, has not been well studied. The utility of specific pharmacotherapies in women, different ethnic/racial groups, adolescent and geriatric patients, and individuals with co-morbid alcohol and drug use disorders (including nicotine dependence) is also largely unknown, as is the appropriateness of medication therapy for treatment of early problem drinkers. The ultimate aim of these efforts is the development of algorithms for the pharmacological treatment of heavy drinking, which incorporate the characteristics of the patient and of pharmacological and psychosocial treatments with demonstrated efficacy. Although a general framework for such an effort currently exists, much detail is needed before it will be of widespread clinical value.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/537
http://dx.doi.org/10.1093/alcalc/35.6.537
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Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/5482015-05-19HighWireOUPalcalc:35:6
EFFECTS OF ETHANOL ON EXTRACELLULAR AMINO ACID LEVELS IN HIGH-AND LOW-ALCOHOL SENSITIVE RATS: A MICRODIALYSIS STUDY
Dahchour, Abdelkader
Hoffman, Alex
Deitrich, Richard
de Witte, Philippe
ORIGINAL ARTICLES
Selectively bred high-alcohol sensitive (HAS) and low-alcohol sensitive (LAS) rats possess a number of behavioural and electrophysiological differences in their responses to alcohol. Using a microdialysis technique, we have evaluated whether the levels of the amino acids aspartate, glutamate, arginine, taurine, and alanine in HAS and LAS rats differ in their response to ethanol administration (2 g/kg, i.p.). The basal concentrations of each amino acid in these two groups were statistically similar. Following ethanol injection, alanine, arginine, and glutamate were significantly decreased in HAS rats, whereas, alanine, glutamate, and taurine were significantly increased in LAS rats by the end of the experiment. Interestingly, an increase in the sulphonated amino acid taurine was only evident 20 min after ethanol administration in the HAS rats, when compared to saline controls. No changes were observed in the other amino acids studied, aspartate and glycine, after ethanol administration. These data suggest that, in addition to differential behavioural responses to alcohol, HAS and LAS rats also differ in their neurochemical responses to ethanol.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/548
http://dx.doi.org/10.1093/alcalc/35.6.548
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Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/5542015-05-19HighWireOUPalcalc:35:6
INFLUENCE OF CHRONIC ALCOHOL INGESTION ON ACETALDEHYDE-INDUCED DEPRESSION OF RAT CARDIAC CONTRACTILE FUNCTION
Ren, Jun
Brown, Ricardo A.
ORIGINAL ARTICLES
Long-standing ethanol consumption acts as a chronic cardiac stress and often leads to alcoholic cardiomyopathy. We have recently shown that the acute ethanol-induced depression in myocardial contraction was substantiated by chronic ethanol ingestion. Acetaldehyde (ACA), the main ethanol metabolite, has been considered to play a role in ethanol-induced cardiac dysfunction. To evaluate the ACA-induced cardiac contractile response following chronic ethanol ingestion, mechanical properties were examined using left ventricular papillary muscles and myocytes from rats fed with control or ethanol-enriched diet. Muscles and myocytes were electrically stimulated at 0.5 Hz and contractile properties analysed included peak tension development (PTD) and peak shortening (PS). Intracellular Ca2+ transients were measured as fura-2 fluorescence intensity changes (ΔFFI). Papillary muscles from ethanol-consuming animals exhibited reduced baseline PTD and attenuated responsiveness to increase of extracellular Ca2+. Acute ACA (0.3–10 mM) addition elicited a dose-dependent depression of PTD. However, the inhibition magnitude was significantly reduced in ethanol-treated rats. Myocytes from both control and ethanol-treated rats exhibited comparable ACA-induced depression in both PS and ΔFFI. Collectively, these data suggest that the ACA-induced depression of myocardial contraction is reduced at the multicellular level, but unchanged at the single cell level, following chronic ethanol ingestion.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/554
http://dx.doi.org/10.1093/alcalc/35.6.554
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Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/5612015-05-19HighWireOUPalcalc:35:6
ACETALDEHYDE PRODUCTION AND METABOLISM BY HUMAN INDIGENOUS AND PROBIOTIC LACTOBACILLUS AND BIFIDOBACTERIUM STRAINS
Nosova, T.
Jousimies-Somer, H.
Jokelainen, K.
Heine, R.
Salaspuro, M.
ORIGINAL ARTICLES
Many human gastrointestinal facultative anaerobic and aerobic bacteria possess alcohol dehydrogenase (ADH) activity and are therefore capable of oxidizing ethanol to acetaldehyde. We examined whether human gastrointestinal lactobacilli (three strains), bifidobacteria (five strains) and probiotic <it>Lactobacillus</it> GG ATCC 53103 are also able to metabolize ethanol and acetaldehyde <it>in vitro</it>. Acetaldehyde production by bacterial suspensions was determined by gas chromatography after a 1-h incubation with 22 mM ethanol. To determine the acetaldehyde consumption, the suspensions were incubated with 50 μM or 500 μM acetaldehyde as well as with 500 μM acetaldehyde and 22 mM ethanol, i.e. under conditions resembling those in the human colon after alcohol intake. The influence of growth media and bacterial concentration on the ability of lactobacilli to metabolize acetaldehyde and to produce acetate from acetaldehyde were determined. ADH and aldehyde dehydrogenase (ALDH) activities were determined spectrophotometrically. Neither measurable ADH nor ALDH activities were found in aerobically grown <it>Lactobacillus</it> GG ATCC 53103 and <it>Lactobacillus acidophilus</it> ATCC 4356 strains. All the lactobacilli and bifidobacteria strains revealed a very limited capacity to oxidize ethanol to acetaldehyde <it>in vitro. Lactobacillus</it> GG ATCC 53103 had the highest acetaldehyde-metabolizing capacity, which increased significantly with increasing bacterial concentrations. This was associated with a marked production of acetate from acetaldehyde. The type of the growth media had no effect on acetaldehyde consumption. Addition of ethanol to the incubation media diminished the acetaldehyde-metabolizing capacity of all strains. However, in the presence of ethanol, <it>Lactobacillus</it> GG ATCC 53103 still demonstrated the highest capacity for acetaldehyde metabolism of all strains. These data suggest a beneficial impact of <it>Lactobacillus</it> GG ATCC 53103 on high gastrointestinal acetaldehyde levels following alcohol intake. The possible clinical implications of this finding remain to be established in <it>in vitro</it> studies.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/561
http://dx.doi.org/10.1093/alcalc/35.6.561
en
Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/5692015-05-19HighWireOUPalcalc:35:6
ACTIVATION OF NEUTRAL SPHINGOMYELINASE PARTICIPATES IN ETHANOL-INDUCED APOPTOSIS IN HEP G2 CELLS
Liu, Jian-Jun
Wang, Ji-Yao
Hertervig, Erik
Cheng, Yajun
Nilsson, Åke
Duan, Rui-Dong
ORIGINAL ARTICLES
The mechanism underlying ethanol-induced apoptosis in liver cells is not clear. Sphingomyelin (SM) metabolism is a novel signal transduction pathway that has an impact on apoptosis in many cell types. We investigated whether the SM pathway is involved in ethanol-induced apoptosis in the liver. Hep G2 cells were treated with ethanol followed by assaying apoptosis, sphingomyelinase (SMase) activity, caspase-3 activity, and the changes of SM content in the cells. We found that ethanol dose-dependently increased apoptosis and the effect was accompanied by increases of caspase-3 activity and neutral SMase activity. At concentrations of 80 and 160 mM, ethanol significantly increased caspase-3 activity by 120% and neutral SMase activity by 24%. The activity of acid SMase was only slightly increased without statistical significance. C<inf>2</inf>-ceramide, the exogenous SM metabolite, mimicked the effects of ethanol on apoptosis and caspase-3 activation. When the SM content was determined 24 h after treatment with ethanol, its level was 15% lower than that of controls. The results indicate that metabolism of SM triggered by neutral SMase participates in ethanol-induced apoptosis in Hep G2 cells and activation of caspase-3 is involved in the apoptotic pathway.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/569
http://dx.doi.org/10.1093/alcalc/35.6.569
en
Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/5742015-05-19HighWireOUPalcalc:35:6
PROBLEM DRINKING AMONG HOSPITALIZED PATIENTS IN HUNGARY
Varvasovszky, Zsusza
McKee, Martin
ORIGINAL ARTICLES
Alcohol is an important determinant of the overall burden of disease in Eastern Europe. It is a particularly important problem in Hungary, where death rates from cirrhosis have increased rapidly to levels much higher than in neighbouring countries. This study sought to describe the prevalence of problem drinking among the hospitalized population in Hungary by means of a survey of self-reported alcohol consumption and of the prevalence of current or lifetime problem drinking among hospitalized patients in the four teaching hospitals in Hungary. A survey was conducted of all patients (<it>n</it> = 3140) admitted to medical, surgical, trauma, psychiatric and neurological wards over a 2-week period in 1997 who stayed in hospital for at least 24 h, using a survey instrument based on the Alcohol Use Disorders Identification Test (AUDIT) and Luebeck Alcoholism Screening Test (LAST) instruments designed to screen for current and lifetime problem drinking respectively. In all, 23.5% of men and over 53.5% of women reported never drinking alcohol. Of those who did drink, about one in eight men and less than 1% of women reported drinking 5 or more drinks on a day when they drank. Whether defined by LAST or AUDIT, the prevalence of problem drinking was ~19% among men and 2% among women, although this rose to 32–35% among men aged 35–44 years. The rate did not vary significantly with employment or education, but was higher among those who were divorced. These high rates of problem drinking indicate the need for coherent policies on alcohol in Hungary.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/574
http://dx.doi.org/10.1093/alcalc/35.6.574
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Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/5802015-05-19HighWireOUPalcalc:35:6
OUTCOME AFTER IN-PATIENT DETOXIFICATION FOR ALCOHOL DEPENDENCE: A NATURALISTIC COMPARISON OF 7 VERSUS 28 DAYS STAY
Foster, J. H.
Marshall, E. J.
Peters, T. J.
ORIGINAL ARTICLES
Research has tended to show that the gains of residential rehabilitation are short-term and cost-inefficient. This study compares the outcomes of two samples, one group staying at a non-statutory sector alcohol detoxification unit for ≤7 days (short stay: SS) with a second group also admitted for detoxification but who stayed at the Unit for a further 8–21 days (long stay: LS). Allocation was not at random: the longer stay was either at the request of the client, referring or treatment agency itself and then had to be approved by an external funding agency. Sixty-four DSM-IV (<it>Diagnostic and Statistical Manual of Mental Disorders</it>) alcohol-dependent subjects were studied. Baseline data included socio-demographic information, illicit drug use during the past 12 months, severity of alcohol dependence, alcohol problems, physical/psychological symptoms, depression and indices of quality of life. At baseline, LS subjects reported more recreational cannabis use than SS subjects. Sixty-two (97%) subjects were re-interviewed 12 weeks after baseline assessment. During follow-up, equal proportions of each group relapsed (≥21 units/7 day period for males; ≥14 units/7day period for females). There was a trend for SS clients to have consumed less alcohol in total than the LS clients. The trend was towards improvement in the study measurements for the SS group, though none of the changes was significant. In the LS group, all variables tended towards a deterioration in health status. The longer stay did not appear to confer any extra benefit to the LS group. Cannabis use and illicit drug use at baseline, while commoner in the LS group, did not predict drinking or social adjustment in the follow-up period in this sample and thus could not be used to explain the lack of a better outcome in the LS group.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/580
http://dx.doi.org/10.1093/alcalc/35.6.580
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Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/5872015-05-19HighWireOUPalcalc:35:6
A MULTICENTRE, RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED TRIAL OF NALTREXONE IN THE TREATMENT OF ALCOHOL DEPENDENCE OR ABUSE
Chick, Jonathan
Anton, Raymond
Checinski, Ken
Croop, Robert
Drummond, D. Colin
Farmer, Roger
Labriola, Dominic
Marshall, Jane
Moncrieff, Joanna
Morgan, Marsha Y.
Peters, Timothy
Ritson, Bruce
ORIGINAL ARTICLES
The opioid antagonist, naltrexone, is reported, in single centre studies, to improve the clinical outcome of individuals with alcohol dependence participating in outpatient psychosocial programmes. This is the first multicentre controlled study to evaluate the efficacy and safety of naltrexone as adjunctive treatment for alcohol dependence or abuse. Patients who met criteria for alcohol dependence (<it>n</it> = 169) or alcohol abuse (<it>n</it> = 6) were randomly assigned to receive double-blind oral naltrexone 50 mg daily (<it>n</it> = 90) or placebo (<it>n</it> = 85) for 12 weeks as an adjunct to psychosocial treatment. The primary efficacy variable was time to first episode of heavy drinking; secondary efficacy assessments included time to first drink, alcohol consumption, craving, and changes in the serum biological markers gamma-glutamyl transferase (GGT), and aspartate and alanine aminotransferases. Compliance was assessed by tablet counts and, in the naltrexone-treated group, by measurement of urinary concentrations of 6-β-naltrexol. Forty-nine (58%) patients randomized to placebo and 53 (59%) randomized to naltrexone did not complete the study. In intention-to-treat analyses, there was no difference between groups on measures of drinking. The median reduction from baseline of serum GGT (<it>P</it> < 0.05) and the reductions in alcohol craving (Obsessive and Compulsive Drinking Scale: OCDS) were greater in the naltrexone group (<it>P</it> < 0.05), from approximately half-way through the study. Of 70 patients (35 placebo; 35 naltrexone) who met an <it>a priori</it> definition of compliance (80% tablet consumption, attendance at all follow-up appointments), those allocated to naltrexone reported consuming half the amount of alcohol (<it>P</it> < 0.05), had greater median reduction in serum GGT activity (<it>P</it> < 0.05), and greater reduction in alcohol craving (OCDS total score: <it>P</it> < 0.05; Obsessive subscale score: <it>P</it> < 0.05), compared to patients in the placebo group. Use of naltrexone raised no safety concerns. Naltrexone is effective in treating alcohol dependence/abuse in conjunction with psychosocial therapy, in patients who comply with treatment.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/587
http://dx.doi.org/10.1093/alcalc/35.6.587
en
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oai:open-archive.highwire.org:alcalc:35/6/5942015-05-19HighWireOUPalcalc:35:6
EFFECTS OF ALCOHOL AND THE EVENING MEAL ON SHEAR-INDUCED PLATELET AGGREGATION AND URINARY EXCRETION OF PROSTANOIDS
Numminen, Heikki
Kobayashi, Michiko
Uchiyama, Shinichiro
Iwata, Makoto
Ikeda, Yasuo
Riutta, Asko
Syrjälä, Martti
Kekomäki, Riitta
Hillbom, Matti
ORIGINAL ARTICLES
Moderate regular alcohol intake has been found to be associated with a decreased risk for coronary heart disease and stroke. We investigated the effects of acute intake of red wine (60 g ethanol) and a standard dinner under controlled conditions on haemostatic factors. Shear-induced platelet aggregation (SIPA) decreased after the intake of alcohol irrespective of whether the subjects were fasting or not, and also after the intake of food. The intake of alcohol inhibited the postprandial increase of von Willebrand factor multimers. Plasma levels of plasminogen activator inhibitor 1 activity (PAI-1) and serum triglycerides were increased by alcohol. Excretion of the platelet thromboxane A<inf>2</inf> metabolites 11-dehydrothromboxane B<inf>2</inf> and 2,3-dinorthromboxane B<inf>2</inf>, as well as the endothelial prostacyclin metabolite 2,3-dinor-6-ketoprostaglandin F<inf>1</inf>&agr;, into urine was not influenced by either alcohol or food. We conclude that eating a dinner together with red wine has no untoward effect on SIPA and that the decrease of SIPA is not specific for alcohol.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/594
http://dx.doi.org/10.1093/alcalc/35.6.594
en
Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/6012015-05-19HighWireOUPalcalc:35:6
QUANTIFICATION OF ALCOHOL-RELATED MORTALITY IN SWEDEN
Sjögren, Harmeet
Eriksson, Anders
Broström, Göran
Ahlm, Kristin
ORIGINAL ARTICLES
The main aim of the present study was to estimate total alcohol-related mortality in Sweden. For natural deaths, a meta-analysis carried out in Australia was updated to the end of March 1998, and pooled estimates of the relative risks were calculated for different diseases based on data from scientific studies that have been published in the international literature. The proportion of current alcohol drinkers from recent Swedish surveys, and the pooled relative risk estimates were used to estimate disease-specific alcohol-attributable fractions. Natural deaths ‘caused’ or ‘prevented’ by alcohol were estimated for the period 1992–1996. For unnatural deaths, all cases from 1992 through 1996 in Sweden were analysed (<it>n</it> = 23 132). Alcohol was regarded to attribute to the death: if the deceased was a ‘known alcoholic’; if the underlying or contributing cause of death was alcohol-related; if the deceased had an alcohol-related in-patient diagnosis during a 3-year period prior to death; if the case tested positive for blood alcohol. Person years of life lost/gained (<70 years) due to alcohol were also assessed. The assumptions underlying the attributable risk methods used to analyse alcohol-related mortality due to natural causes need to be borne in mind when interpreting the results on natural deaths. Moreover, the preventive effect of alcohol on coronary heart disease and stroke is still controversial. The findings of alcohol-related mortality due to unnatural causes were much more reliable. About 3.5% of deaths were attributed to alcohol; alcohol involvement was more than twice as common in deaths of males (4.8%) than in those of females (2.0%). About one-quarter of the deaths in those aged below 50 years were attributed to alcohol. In those (≤69 years, alcohol had a net harmful effect in that it ‘caused’ more deaths than it ‘prevented’; 7% of deaths were in net ‘caused’. More person years of life were in net lost than were saved by alcohol, suggesting that alcohol has a negative effect on premature mortality. We conclude that alcohol accounted for about 3.5% of deaths in all ages, and 25% of deaths in those aged below 50 years, and about 10% of person years of life lost in Sweden. The balance of harm and benefit does not weigh in favour of making a recommendation to the public to drink in order to prevent death.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/601
http://dx.doi.org/10.1093/alcalc/35.6.601
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Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/6122015-05-19HighWireOUPalcalc:35:6
MECHANISMS OF HYPONATRAEMIA IN ALCOHOL PATIENTS
Liamis, George L.
Milionis, Haralampos J.
Rizos, Evangelos C.
Siamopoulos, Kostas C.
Elisaf, Moses S.
ORIGINAL ARTICLES
Hyponatraemia is commonly reported in chronic alcoholic patients. However, the underlying pathogenetic mechanisms are not well delineated. In the current study, we analysed the possible pathophysiological mechanisms of hyponatraemia in a group of alcoholic patients (<it>n</it> = 127) admitted to our hospital for causes related to alcohol misuse. Hyponatraemia (serum sodium <134 mmol/l) was found in 22 patients (17.3%). The most common cause of hyponatraemia in our cohort was hypovolaemia (12 patients); pseudohyponatraemia was diagnosed in six patients with alcohol-induced severe hypertriglyceridaemia. It is of interest that two patients fulfilled the criteria of the so-called ‘beer potomania’ syndrome, while in two others, hyponatraemia was due to reset osmostat or to cerebral salt wasting syndrome, not previously described in alcoholic patients. It is concluded that hyponatraemia is a frequently observed electrolyte disorder in hospitalized alcoholic patients and is related to various pathophysiological mechanisms.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/612
http://dx.doi.org/10.1093/alcalc/35.6.612
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oai:open-archive.highwire.org:alcalc:35/6/6172015-05-19HighWireOUPalcalc:35:6
AUTONOMIC REACTIVITY TO MENTAL STRESSORS AFTER SINGLE ADMINISTRATION OF LORAZEPAM IN MALE ALCOHOLICS AND HEALTHY CONTROLS
Demmel, Ralf
Rist, Fred
Olbrich, Robert
ORIGINAL ARTICLES
Clinically unaffected sons of male alcoholics differ from controls without a family history of alcoholism in two respects: increased autonomic reactivity to aversive as well as non-aversive stimuli and increased attenuation of these responses by alcohol. This pattern of autonomic hyper-reactivity and alcohol-induced stress response dampening (SRD) might be a trait marker of genetic vulnerability and is often interpreted in terms of a diathesis stress model of alcohol dependence. Forty-five alcohol-dependent men (mean age: 39.20 years) and 37 healthy controls (mean age: 35.03 years) participated in a double-blind cross-over study in two experimental sessions each. The benzodiazepine lorazepam was selected as an alcohol substitute. Autonomic reactivity and lorazepam-induced SRD were assessed during incentive and non-incentive reaction time tasks as well as mental arithmetics. Alcohol-dependent men showed elevated resting heart rate levels and increased number of non-specific electrodermal responses. Evidence for autonomic hyper-reactivity was found for a subgroup of alcoholics with a family history of alcoholism.
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/617
http://dx.doi.org/10.1093/alcalc/35.6.617
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Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/6252015-05-19HighWireOUPalcalc:35:6
A MEASURE OF THE INTENSITY OF RESPONSE TO ALCOHOL TO SCREEN FOR ALCOHOL USE DISORDERS IN PRIMARY CARE
Daeppen, Jean-Bernard
Landry, Ulrika
Pécoud, Alain
Decrey, Hedi
Yersin, Bertrand
ORIGINAL ARTICLES
Alcohol-dependent subjects tend to report lower level of response to alcohol (LR) in the years before the disorder developed, compared to control subjects. The Self-Rating of the Effects of alcohol (SRE) score is a quick and valid retrospective estimate of LR. This study examined the associations between alcohol abuse or dependence and early experience of alcohol as measured on retrospective SRE score (relating to the first five times alcohol was imbibed), and the presence of alcohol abuse or dependence, in patients attending primary care. Higher Early SRE score (i.e. greater early tolerance of alcohol) was obtained in patients with an alcohol-related diagnosis than in patients without those diagnoses. Using a cut-off of 2 on the Early SRE score, the Early SRE score could discriminate between patients with and without an alcohol diagnosis with moderate to high sensitivity (84%) and modest specificity (57%).
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/625
http://dx.doi.org/10.1093/alcalc/35.6.625
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Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/628-a2015-05-19HighWireOUPalcalc:35:6
Alcohol and Alcoholism. Effects on Brain and Development.: Edited by J. H. Hannigan, L. P. Spear, N. E. Spear, C. R. Goodlett. Lawrence Erlbaum Associates, Mahway, NJ. 1999. ISBN: 0805826866.
Farmer, R.
BOOK REVIEWS
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/628-a
http://dx.doi.org/10.1093/alcalc/35.6.628-a
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Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/628-b2015-05-19HighWireOUPalcalc:35:6
Drugs and Alcohol Policies.: By Tricia Jackson. Institute of Personnel and Development, London. 1999, 106 pp., {pound}9.99. ISBN: 0-85292-811-4. Available from Plymbridge Distributors or from the IPD website: www.ipd.co.uk.
McCann, M. G.
BOOK REVIEWS
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/628-b
http://dx.doi.org/10.1093/alcalc/35.6.628-b
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oai:open-archive.highwire.org:alcalc:35/6/6282015-05-19HighWireOUPalcalc:35:6
Alcohol and the Community: A Systems Approach to Prevention.: By Harold Holder. Cambridge University Press, Cambridge. 1999, 183pp. including index, {pound}45. ISBN: 0521591872.
Ritson, Bruce
BOOK REVIEWS
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/628
http://dx.doi.org/10.1093/alcalc/35.6.628
en
Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/629-a2015-05-19HighWireOUPalcalc:35:6
The Treatment of Drinking Problems. A Guide for the Helping Professions.: By Griffith Edwards and E. Jane Marshall. Cambridge University Press, Cambridge. 1997, 380pp., {pound}24.95. ISBN: 0521497930.
Daly, Chris
BOOK REVIEWS
Oxford University Press
2000-11-01 00:00:00.0
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/629-a
http://dx.doi.org/10.1093/alcalc/35.6.629-a
en
Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/629-b2015-05-19HighWireOUPalcalc:35:6
Community Treatment of Drug Misuse: More than Methadone.: By Nicholas Seivewright. Cambridge University Press, Cambridge. 1999, 260pp., {pound}22.95. ISBN: 0521665620.
Garvey, Tim
BOOK REVIEWS
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/629-b
http://dx.doi.org/10.1093/alcalc/35.6.629-b
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oai:open-archive.highwire.org:alcalc:35/6/6292015-05-19HighWireOUPalcalc:35:6
Counselling Addicted Women.: By M. Cohen. Sage Publications Ltd. 1999, 224pp., {pound}25. ISBN: 0761909109.
Plant, Moira
BOOK REVIEWS
Oxford University Press
2000-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/629
http://dx.doi.org/10.1093/alcalc/35.6.629
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Copyright (C) 2000, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:35/6/6302015-05-19HighWireOUPalcalc:35:6
Alcohol use among Adolescents.: By M. Windle. Sage Publications. 1999, 160pp., {pound}15.99. ISBN: 0761909206.
Firth, David
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Oxford University Press
2000-11-01 00:00:00.0
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http://alcalc.oxfordjournals.org/cgi/content/short/35/6/630
http://dx.doi.org/10.1093/alcalc/35.6.630
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Copyright (C) 2000, Medical Council on Alcohol