Joint influence of alcohol, tobacco, and coffee on biological markers of heavy drinking in alcoholics.

Background: Recent reports suggest that gamma-glutamyl transferase (GGT) decreases with coffee intake. The aim of this study was to examine the joint influence of alcohol, tobacco, cotinine, coffee, and caffeine on biological markers of heavy drinking in an alcoholic population.

Methods: Subjects were 160 alcohol-dependent inpatients.

How useful is aminolevulinic acid dehydratase as a marker of recent alcohol intake?

Erythroycte delta aminolevulinic acid dehydratase (ALAD) has been suggested as a marker for detecting recent alcohol intake. Unlike other markers, ALAD activity decreases after alcohol intake. Review of the literature suggests that the main interest in this marker is because it increases rapidly after withdrawal.

[Depression and smoking].

Lifetime history of major depressive disorder is more than double in ever smokers than in never smokers. Conversely, adjusted odds ratios of nicotine dependence are significantly elevated for major depressive disorder alone (3,11) or associated with an anxiety disorder (4,38). There is also a significant relationship between depressive symptoms' severity (CES-D) and ever smoking.

Double-blind randomized multicentre trial of acamprosate in maintaining abstinence from alcohol.

A prospective placebo-controlled, randomized double-blind study of Acamprosate at two dose levels in alcohol-dependent patients followed up for 12 months was performed. After detoxification, each of the 538 patients included was randomly assigned to one of three groups: 177 patients received placebo, 188 received Acamprosate at 1.3 g/day (low dose group) and 173 received 2.

[Physiopathology of acute alcoholic intoxication and alcoholic withdrawal].

Ethanol blood levels are the result of alcohol absorption and the process of its distribution, metabolism and excretion. Kinetics are complex and not yet well known. They can be influenced by acquired factors (type of alcohol ingested, association with fasting or eating, induction or inhibition of ethanol metabolism) or by genetically determined differences in the activity of alcohol and of acetaldehyde dehydrogenase.

[Acute alcoholic intoxication and drugs].

Acute alcohol ingestion can induce drug interactions, either pharmacokinetic or pharmacodynamic. Metabolically, they especially result from interference in the enzymatic systems which catalyse ethanol oxidation, the blocking of alcohol dehydrogenase, blocking of the microsomal oxidation system of ethanol with accumulation of the xenobiotic and risk of overdose, and blocking of acetaldehyde dehydrogenase with an antabuse effect. Pharmacodynamically, the main interactions result from the action of drugs having a sedative effect, such as tranquilizers but also antidepressants, neuroleptics, analgesics, H1 antihistamines, central antihypertensive drugs (CNS depressant?), etc.

[Alcohol, sleep and biological rhythms].

Alcohol reduces sleep latency but notably alters sleep structure: sleep is fragmented, particularly at the end of the night. Slow wave sleep duration is enhanced in the first part of the night and REM sleep duration and density are diminished. Alcohol withdrawal provokes inverse effects in alcoholic patients: sleep onset is delayed, slow wave sleep durations diminished and REM sleep duration is enhanced.

[Alcohol consumption and primary dilated cardiomyopathy. Comparison with a population of patients with coronary disease].

Alcohol consumption was compared between 23 men admitted to hospital with idiopathic dilated myocardiopathy (DCM) and 46 men with coronary artery disease. Duration of regular daily alcohol, heavy daily alcohol, mean daily alcohol consumption, in particular consumption of wine were higher in patients with DCM. Among the biological markers, only serum levels of immunoglobulin A and bilirubin were increased in pts with DCM.