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Alcohol Consumers (alcohol + consumer)
Selected AbstractsAnxiety and depression among abstainers and low-level alcohol consumers.ADDICTION, Issue 9 2009The Nord-Trøndelag Health Study ABSTRACT Aims The aim of this study was to examine the levels of anxiety and depression among individuals consuming low levels of alcohol. Design Prospective and cross-sectional population-based study. Setting and participants This study employed data from the Nord-Trøndelag Health Survey (HUNT-2, n = 38 930). Measurements Alcohol consumption was measured by self-report of usual alcohol consumption during a 2-week period. Low-level alcohol consumption was defined as self-reported abstainers and non-abstainers currently consuming no alcohol. Anxiety and depression were measured using the Hospital Anxiety and Depression Rating Scale. Potential explanatory variables included somatic illness and symptoms, health-related behaviour, socio-economic status and social activity. In a subsample (n = 20 337), we also looked at the impact of previous heavy drinking among abstainers ('sick-quitting'). Findings A U-shaped association between alcohol consumption and the risk of anxiety and depression was found. Abstention was related to increased odds for both case-level anxiety [1.34, 95% confidence interval (CI) 1.19,1.52] and depression (1.52, 95% CI 1.30,1.77). This association was accounted for partly by adjustments for socio-economic status, social network, somatic illness, age (depression only), gender (anxiety only) and ,sick-quitting'. We also identified significant differences between participants who label themselves as abstainers compared to those who report no usual alcohol consumption, but who do not label themselves as abstainers. Conclusions The risk of case-level anxiety and depression is elevated in individuals with low alcohol consumption compared to those with moderate consumption. Individuals who label themselves as abstainers are at particularly increased risk. This increased risk cannot fully be explained by somatic illness, social activity or ,sick-quitting'. [source] Abstention, alcohol use and risk of myocardial infarction in men and women taking account of social support and working conditions: the SHEEP case,control studyADDICTION, Issue 10 2003Anders Romelsjö ABSTRACT Aims, Very few studies indicating that low,moderate alcohol consumption protects from myocardial infarction (MI) controlled for social support and working conditions, which could confound the findings. Therefore, a first aim was to study the risk of non-fatal and total MI in relation to volume of alcohol consumption and measures of social support and working conditions. A second aim was to analyse the impact of the volume of earlier alcohol use in abstainers. Design, Data came from a case,control study, the Stockholm Heart Epidemiology Program (SHEEP), including first MI among Swedish citizens 45,70 years old. Setting, Stockholm County 1992,94. Participants, There were 1095 cases of MI in men and 471 in women (928 and 372 were non-fatal), and 2339 living controls from the general population. Measurement, Information about alcohol use at different periods in life and job strain, social anchorage and life control besides pre-existing health problems, smoking, physical activity, socio-economic status and marital status was obtained by a questionnaire from the cases and the controls. Findings, In multivariate logistic regression analyses, the relative risk for MI (especially non-fatal) was reduced among alcohol consumers. RR for non-fatal MI was 0.52 (95% confidence intervals 0.32, 0.85) in men with a consumption of 50,69.9 g 100% ethanol/day and 0.21 (95% confidence interval 0.06, 0.77) in women with a consumption of 30 g or more per day (reference category 0.1,5 g 100% ethanol/day). Men who were abstainers during the previous 1,10 years and with an earlier average consumption of 5,30 g 100% ethanol/day had a significantly lower relative risk compared to such abstainers with an earlier higher consumption. Earlier consumption among abstainers may also have an impact on gender differences in MI. Analyses showed positive interaction between abstention and low life-control in women, but only 4% of the female cases were due to this interaction. There were no other interactions between measures of alcohol use and social anchorage, life control and working situations. Conclusion, Alcohol use had a protective impact on MI, with little impact of job strain, social anchorage and life control, giving increased support for a protective impact of low-moderate alcohol use. The level of previous alcohol consumption among male 1,10-year-long abstainers influenced the risk of MI. [source] Alcohol in Moderation, Cardioprotection, and Neuroprotection: Epidemiological Considerations and Mechanistic StudiesALCOHOLISM, Issue 2 2009Michael A. Collins In contrast to many years of important research and clinical attention to the pathological effects of alcohol (ethanol) abuse, the past several decades have seen the publication of a number of peer-reviewed studies indicating the beneficial effects of light-moderate, nonbinge consumption of varied alcoholic beverages, as well as experimental demonstrations that moderate alcohol exposure can initiate typically cytoprotective mechanisms. A considerable body of epidemiology associates moderate alcohol consumption with significantly reduced risks of coronary heart disease and, albeit currently a less robust relationship, cerebrovascular (ischemic) stroke. Experimental studies with experimental rodent models and cultures (cardiac myocytes, endothelial cells) indicate that moderate alcohol exposure can promote anti-inflammatory processes involving adenosine receptors, protein kinase C (PKC), nitric oxide synthase, heat shock proteins, and others which could underlie cardioprotection. Also, brain functional comparisons between older moderate alcohol consumers and nondrinkers have received more recent epidemiological study. In over half of nearly 45 reports since the early 1990s, significantly reduced risks of cognitive loss or dementia in moderate, nonbinge consumers of alcohol (wine, beer, liquor) have been observed, whereas increased risk has been seen only in a few studies. Physiological explanations for the apparent CNS benefits of moderate consumption have invoked alcohol's cardiovascular and/or hematological effects, but there is also experimental evidence that moderate alcohol levels can exert direct "neuroprotective" actions,pertinent are several studies in vivo and rat brain organotypic cultures, in which antecedent or preconditioning exposure to moderate alcohol neuroprotects against ischemia, endotoxin, ,-amyloid, a toxic protein intimately associated with Alzheimer's, or gp120, the neuroinflammatory HIV-1 envelope protein. The alcohol-dependent neuroprotected state appears linked to activation of signal transduction processes potentially involving reactive oxygen species, several key protein kinases, and increased heat shock proteins. Thus to a certain extent, moderate alcohol exposure appears to trigger analogous mild stress-associated, anti-inflammatory mechanisms in the heart, vasculature, and brain that tend to promote cellular survival pathways. [source] Molecular and Cellular Events in Alcohol-Induced Muscle DiseaseALCOHOLISM, Issue 12 2007Joaquim Fernandez-Solà Alcohol consumption induces a dose-dependent noxious effect on skeletal muscle, leading to progressive functional and structural damage of myocytes, with concomitant reductions in lean body mass. Nearly half of high-dose chronic alcohol consumers develop alcoholic skeletal myopathy. The pathogenic mechanisms that lie between alcohol intake and loss of muscle tissue involve multiple pathways, making the elucidation of the disease somewhat difficult. This review discusses the recent advances in basic and clinical research on the molecular and cellular events involved in the development of alcohol-induced muscle disease. The main areas of recent research interest on this field are as follows: (i) molecular mechanisms in alcohol exposed muscle in the rat model; (ii) gene expression changes in alcohol exposed muscle; (iii) the role of trace elements and oxidative stress in alcoholic myopathy; and (iv) the role of apoptosis and preapoptotic pathways in alcoholic myopathy. These aforementioned areas are crucial in understanding the pathogenesis of this disease. For example, there is overwhelming evidence that both chronic alcohol ingestion and acute alcohol intoxication impair the rate of protein synthesis of myofibrillar proteins, in particular, under both postabsorptive and postprandial conditions. Perturbations in gene expression are contributory factors to the development of alcoholic myopathy, as ethanol-induced alterations are detected in over 400 genes and the protein profile (i.e., the proteome) of muscle is also affected. There is supportive evidence that oxidative damage is involved in the pathogenesis of alcoholic myopathy. Increased lipid peroxidation is related to muscle fibre atrophy, and reduced serum levels of some antioxidants may be related to loss of muscle mass and muscle strength. Finally, ethanol induces skeletal muscle apoptosis and increases both pro- and antiapoptotic regulatory mechanisms. [source] Impact of Alcohol Exposure After Pregnancy Recognition on Ultrasonographic Fetal Growth MeasuresALCOHOLISM, Issue 5 2006Nancy S. Handmaker Background: More than 3 decades after Jones and Smith (1973) reported on the devastation caused by alcohol exposure on fetal development, the rates of heavy drinking during pregnancy remain relatively unchanged. Early identification of fetal alcohol exposure and maternal abstinence led to better infant outcomes. This study examined the utility of biometry for detecting alcohol-related fetal growth impairment. Methods: We obtained fetal ultrasound measures from routine ultrasound examinations for 167 pregnant hazardous drinkers who were enrolled in a brief alcohol intervention study. The fetal measures for women who quit after learning of their pregnancies were compared with measures for women who continued some drinking throughout the course of their pregnancies. Because intensity of alcohol consumption is associated with poorer fetal outcomes, separate analyses were conducted for the heavy (average of ,5 drinks per drinking day) alcohol consumers. Fetal measures from the heavy-exposed fetuses were also compared with measures from a nondrinking group that was representative of normal, uncomplicated pregnancies from our clinics. Analyses of covariance were used to determine whether there were differences between groups after controlling for influences of gestational age and drug abuse. Results: Nearly half of the pregnant drinkers abstained after learning of their pregnancies. When women reportedly quit drinking early in their pregnancies, fetal growth measures were not significantly different from a non,alcohol-exposed group, regardless of prior drinking patterns. Any alcohol consumption postpregnancy recognition among the heavy drinkers resulted in reduced cerebellar growth as well as decreased cranial to body growth in comparison with women who either quit drinking or who were nondrinkers. Amphetamine abuse was predictive of larger cranial to body growth ratios. Conclusions: Alterations in fetal biometric measurements were observed among the heavy drinkers only when they continued drinking after becoming aware of their pregnancies. Although the reliance on self-reported drinking is a limitation in this study, these findings support the benefits of early abstinence and the potential for ultrasound examinations in the detection of fetal alcohol effects. [source] Alcohol-Induced Endothelial Changes Are Associated With Oxidative Stress and Are Rapidly Reversed After WithdrawalALCOHOLISM, Issue 10 2005Giorgio Soardo Abstract: Background: Although heavy alcohol drinkers are at an increased risk of developing cardiovascular events, moderate alcohol intake is associated with reduced incidence of cardiovascular death. This paradox might reflect a dose-related effect of different alcohol intakes on endothelial function and this, in turn, might depend on changes in oxidative stress Methods: We tested the effects of alcohol withdrawal in heavy alcohol consumers and compared the plasma levels of endothelin-1, nitric oxide, plasminogen activator inhibitor-1, von Willebrand factor, malondialdehyde, and intracellular glutathione with those of alcoholics that did not modify their alcohol intake and teetotalers. In human endothelial cells that had been cultured for 2 weeks in the presence of different concentrations of ethanol, we assessed the same parameters after withdrawal of ethanol exposure Results: Alcohol increased the levels of endothelin-1, nitric oxide, and plasminogen activator inhibitor-1 and decreased the levels of von Willebrand factor both in vivo and in vitro. These changes were dose dependent, rapidly reversed after withdrawal of exposure, and associated with the presence of increased oxidative stress as indicated by increased levels of both malondialdehyde and intracellular glutathione. Blockade of oxidative stress by incubation of endothelial cells in the presence of oxidants' scavengers prevented the alcohol-induced functional modifications of the endothelium Conclusions: Alcohol affects endothelial function with an effect that is mediated by an activated oxidative stress and is rapidly reversed after withdrawal. Dose-related endothelial responses to different alcohol intakes might translate in either vascular protection or vascular damage. [source] The effect of alcohol on radiographic progression in rheumatoid arthritisARTHRITIS & RHEUMATISM, Issue 5 2010M. J. Nissen Objective Alcohol consumption reduces the risk of development of rheumatoid arthritis (RA) and significantly attenuates the development of erosive arthritis in animal models. It remains unknown whether alcohol consumption influences joint damage progression in RA. This study was undertaken to compare the rates of radiographic damage progression in alcohol drinkers and nondrinkers in a large prospective cohort of patients with RA. Methods All patients in the population-based Swiss Clinical Quality Management in RA registry database with at least 2 sequential radiographs were included. Joint erosions were assessed in 38 joints in the hands and feet using a validated scoring method. The rate of progression of erosions was analyzed using multivariate regression models for longitudinal data and was adjusted for potential confounders. Results The study included 2,908 patients with RA with a mean of 4 sequential radiographs and 3.9 years of followup. A trend toward reduced radiographic progression existed in drinkers compared with nondrinkers, with a mean rate of erosive progression of 0.99% (95% confidence interval [95% CI] 0.89,1.09) and 1.13% (95% CI 1.01,1.26) at 1 year, respectively. Alcohol consumption displayed a J-shaped dose-response effect, with a more favorable evolution in occasional consumers (P = 0.01) and daily consumers (P = 0.001) as compared with nondrinkers, while heavy drinkers demonstrated worse radiographic evolution (P = 0.0001). We found significant effect modification by sex, with male drinkers displaying significantly less erosive progression compared with male nondrinkers (mean 0.86% [95% CI 0.70,1.03] versus 1.35% [95% CI 1.02,1.67]; P = 0.007). Conclusion Our findings indicate a trend toward reduced radiographic progression in alcohol drinkers compared with nondrinkers, specifically in occasional and daily alcohol consumers. In particular, male patients with RA who consume alcohol demonstrate less radiographic progression than do male nondrinkers. [source] | ||||||||||