• Energy Research
• 3. Good health close
• FI close
• CN close
• University of Helsinki close

Abstract Thirty healthy male volunteers drank ethyl alcohol (1.75 g/kg) from 6 p. m. to 9 p. m., which resulted in hangover the next morning, and 10 subjects served as controls. The twenty subjects, who drank alcohol, received glucose or fructose during the same evening (1.0 g/kg) or on the following morning (0.5 g/kg). In the hangover phase psychomotor performance was recorded by a choice reaction test, two coordination tests and an attention test. The intensity of the hangover was graded subjectively and objectively. Blood ethanol, acetaldehyde and glucose concentrations were analysed. The testing procedure was repeated at 8, 10 and 12 a. m. Ethanol, administered alone, increased significantly the number of mistakes on the choice reaction test in hangover phase, but this effect was abolished by the simultaneous administration of sugar. On the other hand, after the combined administration of ethanol and sugars the number of mistakes and mistake percentage on one coordination test were increased. The etiology on the impaired psychomotor skill during the hangover period is probably not directly related to the pathophysiology of the hangover, as there was no correlation between the impairment of the psychomotor performance and the intensity of the hangover of the subjects.

Salaspuro, M. P. & Kesaniemi, Y. A. Intravenous galactose elimination tests with and without ethanol loading in various clinical conditions. Scand. J. Gastroent. 1973, 8, 681-686.Intravenous galact...

Coma and vomiting are the commonest symptoms in young teenagers intoxicated by alcohol. Severe toxicity, manifested as coma, occurs at lower blood alcohol concentrations in young teenagers than in adults. The effect of ethanol on the state of consciousness is directly proportional to blood alcohol concentration. Among children under 5 years of age the risk of hypoglycaemia is increased. A significant risk in acute alcohol intoxication is the rapid development of coma, which in cold environments could lead to fatal hypothermia. Preschool-age children are reported to eliminate ethanol twice as fast as adults, whereas young teenagers eliminate it at the adult rate. The biochemical disturbances in children 11 to 16 years of age with alcohol intoxication resemble those of adults. Mild acidosis of a respiratory or metabolic origin and mild hypokalaemia are common findings in young teenagers. Fluid replacement with glucose-containing fluids and follow-up are generally the only treatments needed for complete recovery. Motives leading to alcohol intoxication are a wish to get drunk, experimenting, problems in human relations, and attempted suicide. The underlying problems are often family-related, such as divorce, an alcoholic parent and a lower socioeconomic group.

The effect of ethanol on the adsorption of strychnine to activated charcoal was studied in vitro at pH 1.2 and 7.0. At high charcoal-drug ratios the adsorption of strychnine was significantly (p less than 0.001) more complete at neutral pH than at pH 1.2. At these ratios ethanol 10% increased (p less than 0.001) the unadsorbed fractions at both pHs. The acute toxicity of oral strychnine in mice was not influenced by ethanol. Activated charcoal (1000 mg/kg) mixed with strychnine prior to the administration increased its LD50 by 410 fold. When ethanol was administered with charcoal and strychnine, the increase in the LD50 was only 220 fold which is significantly (p less than 0.05) less than without ethanol. Accordingly, the concomitant ingestion of ethanol in drug intoxications may slightly impair the antidotal efficacy of oral activated charcoal. Despite this potential reduction of the antidotal efficacy of charcoal in some extreme situations, there should be no hesitation in administering activated charcoal in acute intoxications since it in any case very effectively inhibits the absorption of most drugs.

It is unclear whether suicides by different methods are distinguishable by their sociodemographic or clinical characteristics. We set out to investigate whether completed suicides by different methods show disparities in their sociodemographic and clinical characteristics. Within the National Suicide Prevention Project in Finland, all 1,397 suicides occurring April 1, 1987, through March 31, 1988, were investigated using the psychological autopsy method. Disparities were found in characteristics of suicide completers using different methods. Intoxication suicides were more often female and had a history of both previous attempts and psychiatric treatment, whereas suicides by shooting were the opposite in character. Victims using vehicle exhaust gas were most frequently younger males who had experienced a recent interpersonal loss or other adverse event and committed suicide while intoxicated with alcohol. Thus, typical characteristics associate with certain suicide methods, probably due to differences in availability and acceptability of the methods. Various restrictions on the availability of suicide methods are likely to exert their possible impact on somewhat different subpopulations at risk. In terms of suicide prevention, it seems reasonable to target availability restrictions for certain identifiable groups of potential suicide attempters. For instance, carefulness in the practice of prescribing of intoxicating substances to particular psychiatric patients seems justified.

Twelve healthy male volunteers were treated (double-blind crossover design) with tofisopam (a new 3,4-benzodiazepine), diazepam, or placebo, on 2 consecutive days each. Psychomotor skills were impaired after a single dose of diazepam (10 mg) given on day 1. Measurements on day 2 showed that some tolerance had developed to the diazepam-induced impairment of reactive and coordinative skills, but not to its effects on flicker fusion or on the extraocular muscle balance. Tofisopam failed to impair performance both as a single dose (100 mg) and after repeated doses (100 + 50 + 50 + 100 mg). The subjects felt more fatigue, dizziness, calmness, and passiveness after diazepam than after tofisopam. When either drug was given together with 0.8 g/kg ethanol on day 2, the breath ethanol concentrations were 0.7--1.0 mg/ml and all psychomotor skills were impaired. Diazepam + ethanol particularly impaired memory and learning as well. After this combination the subjects were classified (time anticipation test) as 'disqualified drivers' more often than after placebo. It is concluded that diazepam, as well as either benzodiazepine with ethanol, may reduce the ability to drive vehicles or operate machinery.

Our study aims at comparing in C57/Bl male mice, the impact of repeated injections of baclofen (an agonist of GABAB receptor) or diazepam (a benzodiazepine acting through a positive allosteric modulation of GABAA receptor) administered during the alcohol-withdrawal period on hippocampus-dependent memory impairments and brain regional glucocorticoid dysfunction after a short (1-week) or a long (4-week) abstinence. Hence, mice were submitted to a 6-month alcohol consumption (12%v/v) and were progressively withdrawn to water. Then, after a 1- or 4-weeks abstinence, they were submitted to a contextual memory task followed by measurements of corticosterone concentrations in the dorsal hippocampus (dHPC), the ventral hippocampus (vHPC) and the prefrontal cortex (PFC). Results showed that 1- and 4-week withdrawn mice exhibited a severe memory deficit and a significant abnormal rise of the test-induced increase of corticosterone (TICC) in the dHPC, as compared to water-controls or to mice still under alcohol consumption. Repeated daily systemic administrations of decreasing doses of diazepam (ranged from 0.5 to 0.12 mg/kg) or baclofen (ranged from 1.5 to 0.37 mg/kg) during the last 15 days of the withdrawal period, normalized both memory and TICC scores in the dHPC in 1-week withdrawn animals; in contrast, only baclofen-withdrawn mice showed both normal memory performance and TICC scores in the dHPC after a 4-week withdrawal period. In conclusion, the memory improvement observed in 4-week withdrawn mice administered with baclofen stem from the protracted normalization of glucocorticoid activity in the dHPC, a phenomenon encountered only transitorily in diazepam-treated withdrawn mice.

Ethanol and drugs can affect each other's absorption, distribution, metabolism, and excretion. When ingested together, ethanol can increase drug absorption by enhancing the gastric solubility of drugs and by increasing gastrointestinal blood flow. However, high concentrations of ethanol induce gastric irritation causing a pyloric spasm which in turn may delay drug absorption and/or reduce bioavailability. The 'quality' of the alcoholic beverage, independent of its ethanol content, can contribute to altered absorption of a drug. Ethanol is not bound to plasma proteins extensively enough to modify drug distribution. However, serum albumin levels in chronic alcoholics may be abnormally low so that some drugs, e.g. diazepam, have an increased volume of distribution. In addition to the amount ingested, the duration of regular intake determines the effect of ethanol on drug metabolism. Acute intake of ethanol inhibits the metabolism of many drugs but long term intake of ethanol at a high level (greater than 200g of pure ethanol per day) can induce liver enzymes to metabolise drugs more efficiently. At the present time there are no accurate means, with the possible exception of liver biopsy, to clinically predict the capacity of an alcoholic to metabolise drugs. Several drugs can inhibit the metabolism of ethanol at the level of alcohol dehydrogenase. Individual predisposition determines the severity of this drug-ethanol interaction. During its absorption phase, ethanol inhibits the secretion of antidiuretic hormone and is also able to induce increased excretion of a drug through the kidneys. However, chronic alcoholics with water retention may show reduced excretion of drugs via this route. At the pharmacodynamic level, ethanol can enhance the deleterious effects of sedatives, certain anxiolytics, sedative antidepressants and antipsychotics and anticholinergic agents, on performance. Mechanisms of lethal interactions between moderate overdoses of ethanol and anxiolytics/opiates/sedatives are poorly understood. On the other hand, certain peptides, 'nonspecific' stimulants, dopaminergic agents and opiate antagonists can antagonise alcohol-induced inebriation to a significant degree.

Background: Prenatal alcohol exposure affects brain structure and function. This study examined brain metabolism using magnetic resonance spectroscopy (MRS) and searched for regions of specific vulnerability in adolescents and young adults prenatally exposed to alcohol.Methods: Ten adolescents and young adults with confirmed heavy prenatal alcohol exposure and a diagnosis within the fetal alcohol spectrum disorders (FASD) were included. Three of them had fetal alcohol syndrome (FAS), 3 had partial FAS (PFAS), and 4 had alcohol‐related neurobehavioral disorder (ARND). The control group consisted of 10 adolescents matched for age, sex, head circumference, handedness, and body mass. Exclusionary criteria were learning disorders and prenatal alcohol exposure. Three‐dimensional 1H magnetic resonance spectroscopic imaging (1H MRSI) was performed in the cerebrum and cerebellum. Metabolite ratios N‐acetylaspartate/choline (NAA/Cho), NAA/creatine (Cr) and Cho/Cr, and absolute metabolite intensities were calculated for several anatomic regions.Results: In patients with FASD, lower NAA/Cho and/or NAA/Cr compared with controls were found in parietal and frontal cortices, frontal white matter, corpus callosum, thalamus, and cerebellar dentate nucleus. There was an increase in the absolute intensity of the glial markers Cho and Cr but no change in the neuronal marker NAA.Conclusions: Our results suggest that prenatal alcohol exposure alters brain metabolism in a long‐standing or permanent manner in multiple brain areas. These changes are in accordance with previous findings from structural and functional studies. Metabolic alterations represent changes in the glial cell pool rather than in the neurons.