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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.

Abstract Aims Alcohol exposure during adolescence is associated with both increased risk for alcohol use disorders and anxiety in adulthood. Our present experiments examined this association using alcohol-preferring AA (Alko Alcohol) rats selected for high voluntary alcohol drinking. Methods Two groups of female AA rats acquired alcohol drinking at different ages. We gave the adolescent-onset group free choice to 10% alcohol and water for seven weeks, starting on post-natal day 42 (PND 42), whereas the adult-onset group started drinking alcohol on PND 112. After the 7-week drinking, we withdrew the adolescent group from alcohol for two weeks, followed by another voluntary 7-week drinking period, started at the same age as the adult-onset group. We assessed anxiety-like behaviour repeatedly during alcohol drinking with open field and elevated plus maze tests. At the end of alcohol drinking, we also tested the rats using the light/dark box, stress-induced body temperature test and social dominance test. Results During the first 7-week alcohol drinking, adolescent rats exhibited significantly slower acquisition of alcohol drinking and lower alcohol preference than the adult-onset group. However, when tested at the same age as the adult-onset rats, they displayed identical alcohol intake and preference. We found no alcohol-induced effects on anxiety- or stress-related behaviour in the experimental groups at any time points. Conclusions These data show that the genetically determined phenotype of high alcohol drinking of the female alcohol-preferring AA rats is not associated with a predisposition to develop anxiety-like behaviour following voluntary alcohol exposure, even when initiated during adolescence.

We studied the effects of ethanol and acetaldehyde on myocardial gene expression of atrial natriuretic peptide (ANP) and growth of rats. Combined ethanol and calcium carbimide treatment increased blood-acetaldehyde levels and ANP mRNA levels by 40-60% in 2-8 day experiments, compared to the controls. The results suggest a role for acetaldehyde in the development of alcoholic heart dysfunction.

The metabolome refers to the functional status of the cell, organ or the whole body. Metabolomic methods measure the metabolome (metabolite profile) which can be used to examine disease progression and treatment responses. Here, our aim was to review metabolomics studies examining effects of alcohol use in humans.We performed a literature search using PubMed and Web of Science for reports on changes in the human metabolite profile associated with alcohol use; we found a total of 23 articles published before end of 2018.Most studies had investigated plasma, serum or urine samples; only four studies had examined other sample types (liver, faeces and broncho-alveolar lavage fluid). Levels of 51 metabolites were altered in two or more of the reviewed studies. Alcohol use was associated with changes in the levels of lipids and amino acids. In general, levels of fatty acids, phosphatidylcholine diacyls and steroid metabolites tended to increase, whereas those of phosphatidylcholine acyl-alkyls and hydroxysphingomyelins declined. Common alterations in circulatory levels of amino acids included decreased levels of glutamine, and increased levels of tyrosine and alanine.More studies, especially with a longitudinal study design, or using more varied sample materials (e.g. organs or saliva), are needed to clarify alcohol-induced diseases and alterations at a target organ level. Hopefully, this will lead to the discovery of new treatments, improved recognition of individuals at high risk and identification of those subjects who would benefit most from certain treatments.

Gut-derived endotoxins have been proposed as mediators of the enhancement of ethanol elimination after chronic alcohol administration. We investigated whether chronically elevated blood-endotoxin levels affect the rate of ethanol elimination in a study where endotoxin was administered chronically from an osmotic minipump to rats fed ethanol in a liquid diet. As expected, an acute dose of ethanol (1.2 g/kg body wt, i.p.) was eliminated significantly faster (329+/-11 mg/kg/h) by chronically ethanol-fed animals than by pair-fed controls (285+/-9 mg/kg/h). However, although endotoxin administration significantly elevated blood-endotoxin levels, the rate of ethanol elimination in endotoxin-treated groups was almost identical when compared either to controls (289 vs 285) or to ethanol-fed rats (328 vs 329). We conclude that chronic endotoxin exposure at levels that only resulted in mild hepatic changes, had no effect on the rate of ethanol elimination and that it is unlikely that endotoxins are involved in the induction of the ethanol elimination rate following chronic alcohol administration.

In this study, the effects of ethanol and age on the morphology of the locus coeruleus (LC) and on the severity of ethanol-withdrawal symptoms were studied during a 5-week intermittent ethanol exposure. Young (3-4 months) and old (29-30 months) male Wistar rats were given highly intoxicating doses of ethanol by intragastric intubations for 4 days, followed by a 3-day ethanol-withdrawal period. This 7-day cycle of ethanol exposure and withdrawal was repeated five times. A non-treated group and a sucrose-fed group of both ages were used as control groups. The severity of ethanol-withdrawal symptoms (rigidity, tremor, irritability, hypoactivity) was rated up to 62 h after the last dose of ethanol. The intoxication level was higher in the old, compared with the young, rats, despite the smaller doses of ethanol given to the old animals. There was no significant difference between the age groups in the severity of the ethanol-withdrawal syndrome. The LC quantitative studies were performed using unbiased stereological methods. The results showed that there was no difference between the age groups in the LC total neuron numbers of the non-treated control groups. The 5-week intermittent ethanol exposure significantly reduced the LC neuron numbers and LC neuronal density in the old ethanol-exposed animals, compared with the sucrose-fed control animals. In the young rats, the ethanol-induced neuron loss did not reach statistical significance. According to the ANCOVA, the difference in the ethanol-induced LC neuronal loss between the age groups may be due to the difference in the intoxication levels. Interestingly, the sucrose intubations were also found to decrease the LC neuronal numbers in the young rats, compared with the non-treated young control group. It was concluded that ageing did not significantly affect the severity of ethanol-withdrawal symptoms or ethanol-induced loss of LC neurons in Wistar rats.

To present findings on the kinetics and dynamics of cardiovascular drugs during alcohol withdrawal (AW), compared with that observed in remission.Studies were reviewed and summarized.A single-dose study in alcoholic patients with propranolol, a beta-adrenergic antagonist, showed that the negative inotropic effect was decreased and the bradycardiac effect increased during AW as compared with during early remission. The hypotensive effect of isosorbid dinitrate, commonly used as a vasodilatator, was weaker at the onset of AW, being associated with the decreased bioavailability of the drug. Verapamil, which is a L-type Ca2+ channel antagonist, produced a bradycardiac effect at the onset of AW, but no effect was observed in early remission. The effect was probably due to changes in L-type Ca2+ channels because no differences in verapamil concentrations between AW and early remission were observed.Taken together, AW modifies the dynamics and kinetics of cardiac drugs, which may have an impact on the treatment of alcoholic patients with cardiac diseases.

Serum anterior pituitary hormone levels of genetically selected AA and ANA rats of Wistar origin as well as those of experimentally selected heavy drinkers (HD) and light drinkers (LD) among normal Wistar rats were studied. AA and HD rats consumed high doses while ANA and LD rats preferred low doses of ethanol. Serum thyroid-stimulating hormone (TSH), prolactin and growth hormone (GH) concentrations were measured by specific radio-immuno-assays before chronic ethanol administration, during physical dependence and on subsequent withdrawal. Basal TSH levels and TSH responses to cold were as a rule decreased in the course of ethanol intake and abstinence, whereas the TRH-induced TSH elevation became more consistent than before ethanol. There was no difference in basal prolactin levels between ethanol preferring and non-preferring rats at abstinence, whereas 30 min cold-exposure seemed to decrease them in HD and LD rats. The high prolactin levels before ethanol and during physical dependence appear to be caused by stress factors involved in the blood collecting procedure. GH levels were not significantly different in ANA, AA, LD and HD rats and neither ethanol intake nor subsequent withdrawal consistently modified GH levels. It is concluded that the observed minor alterations in the levels of anterior pituitary hormones hardly play any significant role in the development of alcohol dependence.

The purpose of this prospective study was to determine how subjective measures of binge drinking predict suboptimal subjective health. In order to contribute to the understanding of potential causal mechanisms, we also aimed to determine the factors through which subjective health predicts alcohol-specific hospitalizations.A total of 16,111 alcohol-drinking men and women, aged 20-54 years, participated in the Health and Social Support baseline postal survey in 1998, and also responded to the repeated measurement 5 years later in 2003 (T2). Suboptimal subjective health was defined as self-reported overall health status being fair, rather poor or poor. Subjective measures of binge drinking were frequency of subjective intoxications/drunkenness, frequency of hangovers and frequency of alcohol-induced pass-outs.Frequency of intoxications, hangovers and alcohol-induced pass-outs, all predicted suboptimal subjective health regardless of several potential confounders, including beverage-specific total intake. Those reporting suboptimal subjective health at baseline had a 5-fold odds ratio (5.08, 95% confidence interval: 3.43, 6.48) for alcohol-related hospitalizations, compared with those rating their health above fair, when gender and age were controlled. Binge drinking, together with concurrent symptoms of depression, explained over 50% of this relationship, and when additionally taking into account smoking, over two-thirds of this relation was explained.Mental health is an important mediating factor between binge drinking, suboptimal subjective health and alcohol-specific hospitalizations, and symptoms of depression should therefore be taken into account in prevention of alcohol-related adverse health outcomes.