[Alcohol drinking, alcoholism and risk].
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Alcoholic drinks are capable of triggering a wide range of allergic and allergic-like responses, including rhinitis, itching, facial swelling, headache, cough and asthma. Limited epidemiological data suggests that many individuals are affected and that sensitivities occur to a variety of drinks, including wine, beer and spirits. In surveys of asthmatics, over 40% reported the triggering of allergic or allergic-like symptoms following alcoholic drink consumption and 30 - 35% reported worsening of their asthma. Sensitivity to ethanol itself can play a role in triggering adverse responses, particularly in Asians, which is due mainly to a reduced capacity to metabolize acetaldehyde. In Caucasians, specific non-alcohol components are the main cause of sensitivities to alcoholic drinks. Allergic sensitivities to specific components of beer, spirits and distilled liquors have been described. Wine is clearly the most commonly reported trigger for adverse responses. Sensitivities to wine appear to be due mainly to pharmacological intolerances to specific components, such as biogenic amines and the sulphite additives. Histamine in wine has been associated with the triggering of a wide spectrum of adverse symptoms, including sneezing, rhinitis, itching, flushing, headache and asthma. The sulphite additives in wine have been associated with triggering asthmatic responses. Clinical studies have confirmed sensitivities to the sulphites in wine in limited numbers of individuals, but the extent to which the sulphites contribute to wine sensitivity overall is not clear. The aetiology of wine-induced asthmatic responses may be complex and may involve several co-factors.
High alcohol drinking (HAD) and low alcohol drinking (LAD) rats were tested, in three exposures, for taste reactivity to five concentrations of alcohol (5%, 10%, 20%, 30%, and 40%, v/v), water, and one concentration each of sucrose and quinine. Of the three reactivity exposures, one was done before a 3-week period of continuous access to water and 10% alcohol, the second test was done immediately after the consumption period, and the final reactivity test was done after 1 month of alcohol abstinence. The results showed that the groups did not differ in reactivity on the initial test. After the consumption tests (when the HAD rats consumed significantly more alcohol than the LAD rats), differences in reactivity were found: HAD rats produced significantly more ingestive responses (which promote consumption) and significantly fewer aversive responses (which facilitate fluid rejection) than LAD rats. These differences were maintained even after 1 month of alcohol abstinence. The present data replicate an earlier experiment with alcohol-preferring (P) rats and alcohol-non-preferring (NP) rats, and indicate that the selective breeding process does not produce differences in the innate perception of the taste of alcohol. However, after experience with drinking alcohol, rats selectively bred for high alcohol consumption exhibit a palatability shift reflected by high ingestive responding and little or no aversive responding. Such a shift would clearly contribute to the maintenance of high levels of alcohol consumption.
Selective breeding has been employed to develop high-alcohol-drinking (HAD) and low-alcohol-drinking (LAD) 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). To identify quantitative trait loci (QTLs) contributing to alcohol consumption, reciprocal HAD and LAD matings in conjunction with F1 intercrosses were used to create 459 F2 progeny. Using selective genotyping of 151 F2 progeny with extreme alcohol consumption scores and a novel least squares method developed by Haley et al (1994), five chromosomal regions (1, 5, 10, 12, and 16) were identified with lod scores greater than 2.0. Genotyping of the entire sample of 459 F2 progeny produced maximum lod scores of 3.5 on chromosome 5, 2.4 on chromosome 10, 4.7 on chromosome 12 and 2.9 on chromosome 16. The evidence of linkage to chromosome 1 diminished substantially to a maximum lod score of 0.5 when all F2 progeny were genotyped. This study is the first genome-wide study for QTLs underlying alcohol consumption that has employed noninbred lines. Further localization of these QTLs will likely provide insight and candidate genes for the study of human alcoholism.
PURPOSE: To investigate the characteristics of alcohol use among Japanese adults and prevalence of alcohol dependence in Japan, we conducted a nationwide survey on alcohol drinking behavior and alcohol dependence among Japanese adults using a representative sampling method. METHODS: We sampled 3500 adults from throughout the entire country using a stratified random sampling method with two-step stratification, and carried out a home visit interview survey. A total of 2547 people (72.8%) responded to the survey. The survey period was June, 2003. The questionnaire contained questions about the frequency and quantity of alcohol use, 'hazardous use of alcohol' and 'alcohol dependence' according to the ICD-10 definition, several screening scales on problem use of alcohol (CAGE, KAST, AUDIT), life-time prevalence of 24 alcohol related diseases, smoking status, dysgryphia, and nightcap drinking. RESULTS: The number of respondents was, 1184 males, and 1363 females. Lifetime alcohol drinking, and weekly drinking, and daily drinking rates were 95.1%, 64.4%, and 36.2% for males, 79.0%, 27.5%, and 7.5% for females, respectively. Average daily alcohol consumption was 3.7 units for males, and 2.0 units for females (1 unit = 10 g pure alcohol). The proportion of drinkers who drank alcohol 4 units or more daily was 28.9% for males, and 7.6% for females, and that for 6 units or more was 12.7% for males, and 3.4% for females. The proportion of flasher was 41.2% for males, and 35.0% for females. Among screening questions, problem drinking was most frequently identified using AUDIT (score 12 points or more, 150 persons), followed by KAST (2 points or more, 100 persons) and CAGE (2 points or more, 98 persons). The number of subjects who met the ICD-10 criteria for alcohol dependence was 24, while the number who engaged in hazardous alcohol use was 64. CONCLUSIONS: This study revealed that problem drinking and alcohol dependence are a serious problem in Japanese general population. The problem of females drinking may be growing. The government should emphasize the prevention of alcohol drinking problems in adults and continue the conduct of nationwide prevalence surveys to monitor the problem.
The present review reports on the influence of alcohol drinking and alcohol use disorders on psychiatric disorders and suicidal behaviour. The base of the study was previous reviews of the National Institute on Alcohol Abuse and Alcoholism publication Alcohol and Health in 1993 and by Helgason in 1996. Using a defined search strategy in Medline, another 42 articles from 1994 to 1996 were included in the comorbidity part and 19 in the suicidal part. Epidemiological and clinical studies confirm high comorbidity of substance use disorders and other mental disorders. Alcohol abuse worsens the course of psychiatric disorders. Light to moderate alcohol consumption has no documented positive effect on the course. Levels of risk consumption of alcohol in psychiatric disorders have not been well defined. One-fifth to one-third of increased deaths rate among alcoholics is explained by suicide. In countries with high alcohol consumption, the suicide rate is also high and is increasing with total increased alcohol consumption. Comorbidity is common among suicide victims, and substance use disorders is most frequently combined with depressive disorders. Interpersonal loss within 6 weeks before suicide is more often present among alcoholics than nonalcoholic suicide victims.
The appearance of desialo-transferrin (De-TF) in serum has been reported to be a biochemical marker of chronic alcoholism. However, conclusive evidence of whether De-TF is a marker for chronic alcohol drinking or for alcoholic liver disease (ALD) has not yet been obtained. Glycoproteins can be divided into two groups, a transferrin (TF) group and an alpha 1-acid glycoprotein (A1-AG) group, based on the characteristics of microheterogeneity (M-HTG) of each protein. In the present study, the appearance of M-HTG in serum TF and A1-AG in alcohol drinkers was compared. In 96 patients with ALD, M-HTG of TF was found in 66 patients (68.8%), and M-HTG of A1-AG was found in 61 patients (63.5%). In 20 patients with alcoholic pancreatitis, the detection rate of M-HTG of A1-AG was significantly higher than that of TF. In six patients with pancreatitis but not liver disease, M-HTG of TF was not detected. In 14 alcoholics without liver or pancreas disease, M-HTG of TF was not detected, whereas M-HTG of A1-AG was detected in 6 cases--a significant difference. The amount of alcohol consumed was not different in patients with and without liver disease. In non-ALD, M-HTG of both proteins was detected only in patients with decompensated liver cirrhosis. The detection rate of M-HTG in TF was significantly higher than in A1-AG. These results suggest that M-HTG of serum TF is a marker of ALD and that of serum A1-AG is a marker of chronic alcohol drinking.
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.
BACKGROUND: Low packing density of glial cells, possibly astrocytes, has been described in the prefrontal cortex and hippocampus of "uncomplicated" alcoholics. Astrocytes perform crucial support functions in the processing of neurotransmitters and transfer of energy substrates from blood to cortical neurons. It is still unknown whether attrition in the numbers of astrocytes is only a consequence of prolonged alcohol abuse or also predates the exposure to alcohol in subjects at risk for alcohol dependence. METHODS: We used alcohol-preferring (P) rats exposed ad libitum for 2 or 6 months to either water only or 10% ethanol and alcohol-nonpreferring (NP) rats and nonselected Wistar rats exposed only to water for 2 months. Sections through the rat frontal cortex were immunostained for glial fibrillary acidic protein (GFAP), a specific marker of astrocytes. The packing density of GFAP-immunoreactive (IR) astrocytes and the area fraction of GFAP immunoreactivity were measured in the prelimbic cortex (PLC) using the dissector probe and analysis of binary images of GFAP immunostaining, respectively. RESULTS: The packing density of GFAP-IR astrocytes was significantly lower in both alcohol-naive and alcohol-exposed P rats than in NP rats or Wistar rats. The area fraction of GFAP immunoreactivity was significantly lower in the alcohol-exposed P rats than in NP rats, Wistar rats, and alcohol-naive P rats. CONCLUSION: These results suggest that low density of GFAP-IR astrocytes in the PLC of P rats predates the exposure to alcohol and might be a factor contributing to the increased risk for alcohol dependence. In addition, prolonged free-choice alcohol drinking may reduce the extent of GFAP-IR processes in the PLC of P rats.
It has been documented that ethanol can potentiate brain gamma-aminobutyric acid (GABA)ergic function, and there is a close link between the GABA(A) receptor complex and effects of ethanol, including reinforcement of alcohol which is a fundamental element of alcohol preference. However, it is unknown in what discrete brain regions GABA(A) receptors might be associated with alcohol preference. In the present study, [(35)S]t-butylbicyclophosphorothionate ([(35)S]TBPS) was used to localize GABA(A) receptors in high-alcohol-drinking (HAD) rats and low-alcohol-drinking (LAD) rats which were selectively bred for high and low alcohol preference, respectively. Initial qualitative observations indicated that [(35)S]TBPS binding sites were abundant in many brain areas including the cerebral cortex, hypothalamus and amygdala of HAD and LAD rats. Furthermore, the quantitative autoradiographic analysis revealed fewer [(35)S]TBPS binding sites of GABA(A) receptors in the amygdaloid complex, central medial thalamic nucleus, lateral hypothalamic nucleus and anterior hypothalamic nucleus of HAD rats than LAD rats. Collectively, this study has indicated that HAD rats selectively bred for high alcohol preference possess lower [(35)S]TBPS binding in the brain. Since lower TBPS binding has been proposed to reflect enhanced GABAergic function, as evidenced in rats with seizure or under alcohol withdrawal, the results from the present study suggest that HAD rats might have an enhanced GABAergic function. It is thus likely that enhanced GABAergic function in the brain might be related to high alcohol preference which is characteristic in HAD rats. In addition, the present result showing no difference of [(35)S]TBPS binding in the nucleus accumbens is also in agreement with a notion that [(35)S]TBPS binding may represent only a small spectrum of the GABA(A) receptor complex which is constituted of a sophisticated subunit combination whose functional compositions are still unknown. In conclusion, the present study supports the working hypothesis that GABA(A) receptors are involved in alcohol preference in HAD rats.
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The paper deals with socio-psychological and socio-cultural problems of drunken driving and of alcohol-consumption in general. It is the intention to make evident how the way to show a certain behavior is imbedded in more comprehensive conditions. The contradictory relations between the role of individual traffic and of alcohol consumption in a society on the one hand and the phenomenon of drunken driving on the other hand are pointed out, as well as the different valuation of social drinking and alcohol dependence. The way of profanation of the drug "alcohol" and the importance of social influence on consumption and effect of the drug are shown, taking into consideration the subjective position of the individual in the society. Finally the role of the state and possibilities of a systemic approach against drunken driving are dealt with.
This study showed that alcohol-preferring (P) rats and high alcohol-drinking (HAD) rats possess fewer calcitonin gene-related peptide (CGRP) receptor binding sites than their respective controls in the central amygdaloid nucleus (CeA) which is known to be related to anxiety. Since P and HAD rats are selectively bred for high alcohol preference, and alcohol can produce anxiolytic effect, one can postulate that P and HAD rats preferentially drink alcohol in order to obtain its anxiolytic effect. This study supports a hypothesis that deficit of CGRP receptors in the CeA of P and HAD rats may contribute to alcohol preference.
BACKGROUND: In a previous study, neuropeptide Y (NPY) administered into the lateral ventricles decreased ethanol intake in alcohol-preferring (P) rats but not in alcohol-nonpreferring (NP) or unselected Wistar rats. The purpose of the present investigation is to extend these findings in selectively-bred high-alcohol-drinking (HAD)1 and low-alcohol-drinking (LAD)1 rats by examining the effects of intracerebroventricularly administered NPY on the elevated plus maze test of anxiety and on ethanol and sucrose intake. METHODS: Female HAD1 and LAD1 rats were surgically implanted with cannula into the lateral ventricle. Following recovery, a test of anxiety was conducted in which the rats (n = 12-13/group) received either artificial cerebrospinal fluid (aCSF) or NPY (10 microg) 10 min prior to a 5-min test on an elevated plus maze. Following anxiety testing, 11 HAD and 11 LAD rats were trained to self-administer ethanol (8% w/v), and 5 HAD and 8 LAD rats were trained to self-administer sucrose (2.5%) during daily 2-hr sessions. A within-subject design was used in which the rats were pretreated once a week with aCSF, 5 microg NPY, or 10 microg NPY prior to the drinking sessions. RESULTS: HAD and LAD rats treated with aCSF did not differ in time spent in open arms of the plus maze. NPY increased time spent on the open arms to similar degrees in both rat lines. HAD rats consumed more ethanol and sucrose than LAD rats. NPY increased sucrose intake in both rat lines. However, the same doses of NPY reduced ethanol intake in HAD but not in LAD rats. CONCLUSION: The plus maze results indicated that selective breeding for high and low alcohol preference in the HAD1 and LAD1 rats, respectively, did not yield differences in anxiety-like behavior and in response to the anxiolytic effects of NPY. The increases in sucrose intake were consistent with the known orexigenic effects of NPY. The decreased ethanol intake following NPY administration in HAD rats was similar to previous observations with P rats and is consistent with the hypothesis that ethanol intake and NPY activity may be inversely related.