Problem drinking as intentional risky behavior: Examining the association between state health insurance coverage and excessive alcohol consumption.
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ABSTRACT:
SUBMITTER: Azagba S
PROVIDER: S-EPMC8683933 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:'Omics' techniques are widely used to identify novel mechanisms underlying brain function and pathology. Here we applied a novel metabolomics approach to further ascertain the role of frontostriatal brain regions for the expression of addiction-like behaviors in rat models of alcoholism. Rats were made alcohol dependent via chronic intermittent alcohol vapor exposure. Following a 3-week abstinence period, rats had continuous access to alcohol in a two-bottle, free-choice paradigm for 7 weeks. Nontargeted flow injection time-of-flight mass spectrometry was used to assess global metabolic profiles of two cortical (prelimbic and infralimbic) and two striatal (accumbens core and shell) brain regions. Alcohol consumption produces pronounced global effects on neurometabolomic profiles leading to a clear separation of metabolic phenotypes between treatment groups, particularly. Further comparisons of regional tissue levels of various metabolites, most notably dopamine and Met-enkephalin, allow the extrapolation of alcohol consumption history. Finally, a high-drinking metabolic fingerprint was identified indicating a distinct alteration of central energy metabolism in the accumbens shell of excessively drinking rats that could indicate a so far unrecognized pathophysiological mechanism in alcohol addiction. In conclusion, global metabolic profiling from distinct brain regions by mass spectrometry identifies profiles reflective of an animal's drinking history and provides a versatile tool to further investigate pathophysiological mechanisms in alcohol dependence.
| S-EPMC4367471 | biostudies-other
Project description:BACKGROUND:Genomewide association studies (GWAS) have begun to identify loci related to alcohol consumption, but little is known about whether this genetic propensity overlaps with specific indices of problem drinking in ascertained samples. METHODS:In 6,731 European Americans who had been exposed to alcohol, we examined whether polygenic risk scores (PRS) from a GWAS of weekly alcohol consumption in the UK Biobank predicted variance in 6 alcohol-related phenotypes: alcohol use, maximum drinks within 24 hours (MAXD), total score on the Self-Rating of the Effects of Ethanol Questionnaire (SRE-T), DSM-IV alcohol dependence (DSM4AD), DSM-5 alcohol use disorder symptom counts (DSM5AUDSX), and reduction/cessation of problematic drinking. We also examined the extent to which an single nucleotide polymorphism (rs1229984) in ADH1B, which is strongly associated with both alcohol consumption and dependence, contributed to the polygenic association with these phenotypes and whether PRS interacted with sex, age, or family history of alcoholism to predict alcohol-related outcomes. We performed mixed-effect regression analyses, with family membership and recruitment site included as random effects, as well as survival modeling of age of onset of DSM4AD. RESULTS:PRS for alcohol consumption significantly predicted variance in 5 of the 6 outcomes: alcohol use (?marginal R2 = 1.39%, ? area under the curve [AUC] = 0.011), DSM4AD (?marginal R2 = 0.56%; ?AUC = 0.003), DSM5AUDSX (?marginal R2 = 0.49%), MAXD (?marginal R2 = 0.31%), and SRE-T (?marginal R2 = 0.22%). PRS were also associated with onset of DSM4AD (hazard ratio = 1.11, p = 2.08e-5). The inclusion of rs1229984 attenuated the effects of the alcohol consumption PRS, particularly for DSM4AD and DSM5AUDSX, but the PRS continued to exert an independent effect for all 5 alcohol measures (?marginal R2 after controlling for ADH1B = 0.14 to 1.22%). Interactions between PRS and sex, age, or family history were nonsignificant. CONCLUSIONS:Genetic propensity for typical alcohol consumption was associated with alcohol use and was also associated with 4 of the additional 5 outcomes, though the variance explained in this sample was modest. Future GWAS that focus on the multifaceted nature of AUD, which goes beyond consumption, might reveal additional information regarding the polygenic underpinnings of problem drinking.
| S-EPMC6560626 | biostudies-literature
Project description:IntroductionRisky alcohol consumption (RAC) and heavy episodic drinking (HED) by parents can have negative effects on their children. At present, little is known about these forms of alcohol consumption among parents in Germany. The aim of this analysis is to estimate the percentage of parents living in Germany who practise RAC and HED and to study associations between these consumption patterns and sociodemographic factors.Material and methodsThe data basis comprises the data of the nationwide studies "Gesundheit in Deutschland aktuell" (GEDA) of 2009, 2010, and 2012. The data were collected by means of computer-assisted telephone interviews (CATI). Our analysis included all participants living in a household with at least one child of their own under 18 years of age (n = 16,224). Information on RAC and HED was collected using the AUDIT-C screening instrument. Logistic regression models were used to study the relationship between parental alcohol consumption and sociodemographic variables.Results18.4% of the mothers and 29.6% of the fathers exhibited RAC; 8.4% of the mothers and 21.0% of the fathers practised HED. After mutual adjustment, RAC showed a significant association with the level of education, income (only mothers), employment status (only mothers), migration background, relationship status (only mothers), and the age of the youngest child. HED showed a significant association with income (only mothers), the age of the youngest child (only mothers), and the level of education (only fathers).ConclusionsThe presented analysis emphasizes the relevance of preventive measures to reduce parental alcohol consumption. In addition to universal interventions, risk group-specific measures (e.g., for parents with high income) are needed to reduce parental alcohol consumption and thus support a healthy development of children.
| S-EPMC6915141 | biostudies-literature
Project description:OBJECTIVES:Posttraumatic stress disorder (PTSD) and unhealthy alcohol use are commonly associated conditions. It is unknown whether specific symptoms of PTSD are associated with subsequent initiation of unhealthy alcohol use. METHODS:Data from the first 3 enrollment panels (n?=?151,567) of the longitudinal Millennium Cohort Study of military personnel were analyzed (2001-2012). Complementary log-log models were fit to estimate whether specific PTSD symptoms and symptom clusters were associated with subsequent initiation of 2 domains of unhealthy alcohol use: risky and problem drinking (experience of 1 or more alcohol-related consequences). Models were adjusted for other PTSD symptoms and demographic, service, and health-related characteristics. RESULTS:Eligible study populations included those without risky (n?=?31,026) and problem drinking (n?=?67,087) at baseline. In adjusted analyses, only 1 PTSD symptom-irritability/anger-was associated with subsequent increased initiation of risky drinking (relative risk [RR] 1.05, 95% confidence interval [CI] 1.00-1.09) at least 3 years later. Two symptom clusters (dysphoric arousal [RR 1.17, 95% CI 1.11-1.23] and emotional numbing [RR 1.30, 95% CI 1.22-1.40]) and 5 symptoms (restricted affect [RR 1.13, 95% CI 1.08-1.19], sense of foreshortened future [RR 1.12, 95% CI 1.06-1.18], exaggerated startle response [RR 1.07, 95% CI 1.01-1.13], sleep disturbance [RR 1.11, 95% CI 1.07-1.15], and irritability/anger [RR 1.12, 95% CI 1.07-1.17]) were associated with subsequent initiation of problem drinking. CONCLUSIONS:Findings suggest that specific PTSD symptoms and symptom clusters are associated with subsequent initiation of unhealthy alcohol use.
| S-EPMC6167171 | biostudies-literature
Project description:The present study examined whether parental problem drinking affected parenting (i.e., behavioral control, support, rule-setting, alcohol-specific behavioral control), and whether parental problem drinking and parenting affected subsequent adolescent alcohol use over time. A total of 428 families, consisting of both parents and two adolescents (mean age 13.4 and 15.2 years at Time 1) participated in a three-wave longitudinal study with annual waves. A series of path analyses were conducted using a structural equation modeling program (Mplus). Results demonstrated that, unexpectedly, parental problem drinking was in general not associated with parenting. For the younger adolescents, higher levels of both parenting and parental problem drinking were related to lower engagement in drinking over time. This implies that shared environment factors (parenting and modeling effects) influence the development of alcohol use in young adolescents. When adolescents grow older, and move out of the initiation phase, their drinking behavior may be more affected by other factors, such as genetic susceptibility, and peer drinking.
| S-EPMC2413087 | biostudies-other
Project description:Chronic alcohol abuse has a detrimental effect on the brain and liver. There is no effective treatment for these patients and the mechanism underlying alcohol addiction and consequent alcohol-induced damage of the liver/brain axis remains unresolved. We compared experimental models of alcoholic liver disease (ALD) and alcohol dependence in mice and demonstrated that genetic ablation of IL17 Receptor A (IL17ra-/-), or pharmacological blockade of IL17 signaling effectively suppressed the increased voluntary alcohol drinking in alcohol-dependent mice, and blocked alcohol-induced hepatocellular and neurological damage. The level of circulating IL17A positively correlated with the alcohol use in excessive drinkers, and was further increased in patients with ALD as compared to healthy individuals. Our data suggest that IL17A is a common mediator of excessive alcohol consumption and alcohol-induced liver/brain injury, and targeting IL17A may provide a novel strategy for treatment of alcohol-induced pathology.
2020-04-07 | GSE137228 | GEO
Project description:Previous research demonstrates that the number of problems related to each additional drink consumed on any drinking occasion, dose-response, varies non-linearly across average drinking quantities. We test predictions from a dynamic model of drinking behavior that locates this heterogeneity in drinkers' efforts to equilibrate between costs and benefits of use.Equations derived from the theoretical model are used to assess dose-response across drinking quantity subgroups using censored regressions.Fourteen California, USA, college campuses surveyed from 2003 to 2011.A total of 37?762 undergraduate college students 18 years of age and older.Drinking patterns, five physiological problems related to alcohol use (hangover, memory loss, medical treatment for overdose, nausea/vomiting, passing out) and student demographics.The number of physiological problems related to each additional drink consumed was an inverse function of average drinking quantities (b?=?0.2947, Z?=?21.92, P<0.001), differed by drinker age (of-age drinker b?=?-0.1144, Z?=?-3.95, P < 0.001) and gender (male b?=?-0.3379, Z?=?-18.56, P<0.001) and, at the population level, drinking three drinks per occasion was associated with the greatest number of problems.Among US college students, all drinkers exhibit greater risks for physiological problems related to alcohol use (hangover, memory loss, medical treatment for overdose, nausea/vomiting, passing out) when drinking greater amounts of alcohol, but heavier drinkers (those who consume more on average) exhibit fewer problems for each additional drink consumed (less dose-response) than light and moderate drinkers. Light and moderate drinkers exhibit greater dose-response, with three drinks per occasion associated with the greatest number of problems.
| S-EPMC4437634 | biostudies-other
Project description:Harmful excessive use of alcohol has a severe impact on society and it remains one of the major causes of morbidity and mortality in the population. However, mechanisms that underlie excessive alcohol consumption are still poorly understood, and thus available medications for alcohol use disorders are limited. Here, we report that changing the level of chromatin condensation by affecting DNA methylation or histone acetylation limits excessive alcohol drinking and seeking behaviors in rodents. Specifically, we show that decreasing DNA methylation by inhibiting the activity of DNA methyltransferase (DNMT) with systemic administration of the FDA-approved drug, 5-azacitidine (5-AzaC) prevents excessive alcohol use in mice. Similarly, we find that increasing histone acetylation via systemic treatment with several histone deacetylase (HDAC) inhibitors reduces mice binge-like alcohol drinking. We further report that systemic administration of the FDA-approved HDAC inhibitor, SAHA, inhibits the motivation of rats to seek alcohol. Importantly, the actions of both DNMT and HDAC inhibitors are specific for alcohol, as no changes in saccharin or sucrose intake were observed. In line with these behavioral findings, we demonstrate that excessive alcohol drinking increases DNMT1 levels and reduces histone H4 acetylation in the nucleus accumbens (NAc) of rodents. Together, our findings illustrate that DNA methylation and histone acetylation control the level of excessive alcohol drinking and seeking behaviors in preclinical rodent models. Our study therefore highlights the possibility that DNMT and HDAC inhibitors can be used to treat harmful alcohol abuse.
| S-EPMC3591000 | biostudies-literature
Project description:RationaleEmerging evidence suggests that the ?4?2 form of the nicotinic acetylcholine receptor (nAChR) modulates the rewarding effects of alcohol. The nAChR ?4?2 subunit partial agonist varenicline (Chantix™), which is approved by the Food and Drug Administration for smoking cessation, also decreases ethanol consumption in rodents (Steensland et al., Proc Natl Acad Sci U S A 104:12518-12523, 2007) and in human laboratory and open-label studies (Fucito et al., Psychopharmacology (Berl) 215:655-663, 2011; McKee et al., Biol Psychiatry 66:185-190 2009).ObjectivesWe present a randomized, double-blind, 16-week study in heavy-drinking smokers (n?=?64 randomized to treatment) who were seeking treatment for their smoking. The study was designed to determine the effects of varenicline on alcohol craving and consumption. Outcome measures included number of alcoholic drinks per week, cigarettes per week, amount of alcohol craving per week, cumulative cigarettes and alcoholic drinks consumed during the treatment period, number of abstinent days, and weekly percentage of positive ethyl glucuronide and cotinine screens.ResultsVarenicline significantly decreases alcohol consumption (? (2)?=?35.32, p?<?0.0001) in smokers. Although varenicline has previously been associated with suicidality and depression, side effects were low in this study and declined over time in the varenicline treatment group.ConclusionsVarenicline can produce a sustained decrease in alcohol consumption in individuals who also smoke. Further studies are warranted to assess varenicline efficacy in treatment-seeking alcohol abusers who do not smoke and to ascertain the relationship between varenicline effects on smoking and drinking.
| S-EPMC3438402 | biostudies-literature
Project description:BACKGROUND:Liver damage is a serious and sometimes fatal consequence of long-term alcohol intake, which progresses from early-stage fatty liver (steatosis) to later-stage steatohepatitis with inflammation and fibrosis/necrosis. However, very little is known about earlier stages of liver disruption that may occur in problem drinkers, those who drink excessively but are not dependent on alcohol. METHODS:We examined how repeated binge-like alcohol drinking in C57BL/6 mice altered liver function, as compared with a single binge-intake session and with repeated moderate alcohol consumption. We measured a number of markers associated with early- and later-stage liver disruption, including liver steatosis, measures of liver cytochrome P4502E1 (CYP2E1) and alcohol dehydrogenase (ADH), alcohol metabolism, expression of cytokine mRNA, accumulation of 4-hydroxynonenal (4-HNE) as an indicator of oxidative stress, and alanine transaminase/aspartate transaminase as a measure of hepatocyte injury. RESULTS:Importantly, repeated binge-like alcohol drinking increased triglyceride levels in the liver and plasma, and increased lipid droplets in the liver, indicators of steatosis. In contrast, a single binge-intake session or repeated moderate alcohol consumption did not alter triglyceride levels. In addition, alcohol exposure can increase rates of alcohol metabolism through CYP2E1 and ADH, which can potentially increase oxidative stress and liver dysfunction. Intermittent, excessive alcohol intake increased liver CYP2E1 mRNA, protein, and activity, as well as ADH mRNA and activity. Furthermore, repeated, binge-like drinking, but not a single binge or moderate drinking, increased alcohol metabolism. Finally, repeated, excessive intake transiently elevated mRNA for the proinflammatory cytokine IL-1B and 4-HNE levels, but did not alter markers of later-stage liver hepatocyte injury. CONCLUSIONS:Together, we provide data suggesting that even relatively limited binge-like alcohol drinking can lead to disruptions in liver function, which might facilitate the transition to more severe forms of liver damage.
| S-EPMC5636002 | biostudies-literature