Etoh abuse
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Ethanol Abuse: Insights from Recent Research
Binge Drinking and Ethanol Dependence
Keywords: binge drinking, ethanol dependence, voluntary consumption
Recent studies have explored the effects of binge-like ethanol (EtOH) drinking on subsequent alcohol consumption and dependence. Research using male C57BL/6J mice demonstrated that repeated cycles of binge-like EtOH drinking significantly increased voluntary EtOH intake and preference in later stages, particularly after 6 to 10 binge episodes. However, this history of binge drinking did not affect anxiety-like behaviors, ataxia, or handling-induced convulsions, suggesting that while binge drinking may not immediately induce dependence-like states, it could mark the early stages of dependence1.
Gender Differences in Ethanol Reward Sensitivity
Keywords: gender differences, ethanol reward, ovarian hormones
Gender differences in the rewarding effects of EtOH have been highlighted in studies using place-conditioning procedures in rats. Female rats, both adult and adolescent, exhibited enhanced rewarding effects of EtOH compared to their male counterparts. This heightened sensitivity in females was found to be hormone-dependent, as ovariectomized females did not show the same level of reward. These findings suggest that ovarian hormones play a significant role in the increased vulnerability of females to EtOH abuse2.
Ethanol Abuse and Stroke Outcomes
Keywords: ethanol abuse, stroke, in-hospital outcomes
A 20-year analysis of the Nationwide Inpatient Sample revealed that patients with acute ischemic stroke (AIS) who abused EtOH had worse functional outcomes compared to non-abusers. These patients were more likely to be male, younger, smokers, and have lower socioeconomic status. Despite longer hospital stays, EtOH abuse patients incurred lower hospital charges and were less likely to be discharged home or to short-term hospitals, indicating more severe disease and poorer recovery3.
Co-Abuse of Ethanol and Nicotine
Keywords: ethanol and nicotine co-abuse, mesocorticolimbic system, glutamate activity
The co-abuse of EtOH and nicotine (NIC) has been shown to produce enduring alterations in the brain's reward system. In alcohol-preferring rats, chronic intake of both substances enhanced the rewarding properties of NIC and increased extracellular glutamate levels in the medial prefrontal cortex. These changes suggest that co-abuse of EtOH and NIC can lead to significant neuroplasticity, making relapse more likely during attempts to maintain abstinence4.
Chronic Ethanol Exposure and Compulsive Behavior
Keywords: chronic ethanol exposure, compulsive behavior, glutamatergic transmission
Chronic intermittent EtOH exposure in mice has been linked to increased compulsive-like behaviors, such as persistent EtOH seeking despite punishment. This behavior was associated with increased expression of NMDA receptor subunits and enhanced glutamatergic transmission in the orbitofrontal cortex. These findings indicate that chronic EtOH exposure fosters resistance to negative consequences and promotes compulsive drinking behaviors5.
Age-Dependent Effects of Ethanol on the Brain
Keywords: age-dependent effects, neuroinflammation, astrocyte activation
Ethanol-induced neuroinflammation and glial activation vary with age. In adult mice, EtOH increased the expression of chemokines and cytokines in the brain, while adolescent mice did not show these changes. Both age groups exhibited increased astrocyte activation, suggesting that the neuroimmune response to EtOH is age-specific and may contribute to differential susceptibility to alcohol-induced neuropathology6.
Astrocytes and Ethanol-Induced Calcium Signaling
Keywords: astrocytes, calcium signaling, ethanol exposure
Astrocytes play a crucial role in the brain's response to EtOH. Acute EtOH exposure enhances calcium signaling in astrocytes through a feedback loop involving neuronally-derived purinergic signaling. This interaction highlights the importance of astrocytes in modulating the brain's physiological response to EtOH and their potential role in EtOH-seeking behaviors7.
Oxytocin as a Potential Treatment for Ethanol Abuse
Keywords: oxytocin, ethanol consumption, dopamine release
Oxytocin (OXT) has emerged as a promising treatment for alcohol use disorders. Studies have shown that OXT can reduce voluntary EtOH consumption and block EtOH-induced dopamine release in the nucleus accumbens. This effect on the mesolimbic dopamine pathway may explain the reduced craving and consumption of EtOH following OXT administration8.
Ethanol Metabolism and Behavioral Responses
Keywords: ethanol metabolism, behavioral responses, Caenorhabditis elegans
Research using Caenorhabditis elegans has provided insights into how variations in EtOH metabolism affect behavioral responses. Mutations in genes encoding alcohol dehydrogenase and aldehyde dehydrogenase increased EtOH accumulation and sensitivity to its sedative effects. Additionally, the osmolarity of the EtOH solution significantly influenced the observed sensitivity, indicating that both metabolic and environmental factors play roles in EtOH's behavioral effects9.
Maternal Ethanol Exposure and Offspring Brain Health
Keywords: maternal ethanol exposure, glutamatergic system, oxidative stress
Chronic maternal EtOH consumption during pregnancy and lactation has detrimental effects on the offspring's brain. Studies have shown that such exposure impairs glutamatergic transmission, induces oxidative stress, and leads to energy deficits in the hippocampus of the offspring. These changes are associated with long-term cognitive and behavioral impairments10.
Conclusion
The research on ethanol abuse spans various aspects, from gender differences and co-abuse with nicotine to the effects on brain function and potential treatments. Understanding these diverse impacts is crucial for developing effective interventions and mitigating the adverse effects of ethanol abuse.
Sources and full results
Most relevant research papers on this topic
Repeated cycles of binge-like ethanol (EtOH)-drinking in male C57BL/6J mice augments subsequent voluntary EtOH intake but not other dependence-like phenotypes.
Repeated binge-like ethanol drinking in mice increases voluntary consumption and preference, but does not initially induce dependence-like phenotypes.
Non-RCT
Animal Study
Rigorous Journal
Highly CitedFemale rats display enhanced rewarding effects of ethanol that are hormone dependent.
Human females may be more vulnerable to ethanol abuse due to enhanced rewarding effects mediated by ovarian hormones.
Non-RCTAnimal StudyRigorous JournalHighly CitedAbstract TMP56: Trends In Alcohol Abuse In Patients With Acute Ischemic Stroke: A 20-year Analysis Of The Nationwide Inpatient Sample
Alcohol abuse in acute ischemic stroke patients over 20 years led to higher severity, worse functional outcomes, and lower hospital charges despite longer hospital stays.
Co-administration of ethanol and nicotine: the enduring alterations in the rewarding properties of nicotine and glutamate activity within the mesocorticolimbic system of female alcohol-preferring (P) rats
Chronic ethanol and nicotine co-abuse in female rats enhances nicotine's rewarding properties and increases glutamate levels in the mesocorticolimbic system.
Non-RCTAnimal StudyRigorous JournalChronic EtOH effects on putative measures of compulsive behavior in mice
Chronic intermittent ethanol exposure in mice increases resistance to punished ethanol seeking and alters cortical glutamatergic transmission.
Non-RCTAnimal StudyRigorous JournalEffects of ethanol on immune response in the brain: region-specific changes in adolescent versus adult mice.
Ethanol-induced neuroinflammation and addiction-related molecules show age- and region-specific effects in the brain, with implications for differential alcohol-induced neuropathology and addiction across the life span.
Non-RCTAnimal StudyRigorous JournalHighly CitedAstrocytes promote ethanol-induced enhancement of intracellular Ca2+ signals through intercellular communication with neurons
Astrocytes play a crucial role in shaping the physiological responsiveness to ethanol, enhancing intracellular calcium signals through intercellular communication with neurons.
In Vitro StudyOxytocin inhibits ethanol consumption and ethanol‐induced dopamine release in the nucleus accumbens
Oxytocin infusions can reduce alcohol consumption and ethanol-induced dopamine release in the nucleus accumbens, potentially offering a promising treatment option for alcoholism.
Non-RCTAnimal StudyRigorous JournalHighly CitedEthanol metabolism and osmolarity modify behavioral responses to ethanol in C. elegans.
Ethanol metabolism through ADH and ALDH has a minor influence on sedation and internal accumulation in C. elegans, while osmolarity of the delivery medium significantly affects sensitivity to ethanol.
Rigorous JournalHighly CitedMaternal Exposure to Ethanol During Pregnancy and Lactation Affects Glutamatergic System and Induces Oxidative Stress in Offspring Hippocampus.
Maternal exposure to ethanol during pregnancy and lactation impairs glutamatergic transmission, induces oxidative stress, and causes an energy deficit in offspring hippocampus.
Very Rigorous Journal