Query: cyberbullyin alcohol

title: Increased expression of M1 and M2 phenotypic markers in isolated microglia after four day binge alcohol exposure in male rats.
abstract: Microglia activation and neuroinflammation are common features of neurodegenerative conditions, including alcohol use disorders (AUDs) When activated, microglia span a continuum of diverse phenotypes ranging from classically activated, pro inflammatory (M1) microglia/macrophages to alternatively activated, growth promoting (M2) microglia/macrophages. Identifying microglia phenotypes is critical for understanding the role of microglia in the pathogenesis of AUDs. Therefore, male rats were gavaged with 25% (w/v) ethanol or isocaloric control diet every 8 h for 4 days and sacrificed at 0, 2, 4, and 7 days after alcohol exposure (e.g. T0, T2, etc. Microglia were isolated from hippocampus and entorhinal cortices by Percoll density gradient centrifugation. Cells were labeled with microglia surface antigens and analyzed by flow cytometry. Consistent with prior studies, isolated cells yielded a highly enriched population of brain macrophages/microglia >95% pure) evidenced by staining for the macrophage/microglia antigen CD11b. Polarization states of CD11b+CD45low microglia were evaluated by expression of M1 surface markers, major histocompatibility complex (MHC) II, CD32, CD86, and M2 surface marker, CD206 (mannose receptor) Ethanol treated animals begin to show increased expression of M1 and M2 markers at T0 (p n.s. with significant changes at the T2 time point. At T2, expression of M1 markers, MHC II, CD86, and CD32 were increased (p 0.05) in hippocampus and entorhinal cortices, while M2 marker, CD206, was increased significantly only in entorhinal cortices (p 0.05) All effects resolved to control levels by T4. In summary, four day binge alcohol exposure produces a transient increase in both M1 (MHC II, CD32, and CD86) and M2 (CD206) populations of microglia isolated from the entorhinal cortex and hippocampus. Thus, these findings that both pro inflammatory and potentially beneficial, recovery promoting microglia phenotypes can be observed after a damaging exposure of alcohol are critically important to our understanding of the role of microglia in the pathogenesis of AUDs.

title: The Impact of Brief Alcohol Interventions in Primary Healthcare: A Systematic Review of Reviews
abstract: The aim of the study was to assess the cumulative evidence on the effectiveness of brief alcohol interventions in primary healthcare in order to highlight key knowledge gaps for further research.  An overview of systematic reviews and meta analyses of the effectiveness of brief alcohol intervention in primary healthcare published between 2002 and 2012.  Twenty four systematic reviews met the eligibility criteria (covering a total of 56 randomized controlled trials reported across 80 papers) Across the included studies, it was consistently reported that brief intervention was effective for addressing hazardous and harmful drinking in primary healthcare, particularly in middle aged, male drinkers. Evidence gaps included: brief intervention effectiveness in key groups (women, older and younger drinkers, minority ethnic groups, dependent/co morbid drinkers and those living in transitional and developing countries) and the optimum brief intervention length and frequency to maintain longer term effectiveness.  This overview highlights the large volume of primarily positive evidence supporting brief alcohol intervention effects as well as some unanswered questions with regards to the effectiveness of brief alcohol intervention across different cultural settings and in specific population groups, and in respect of the optimum content of brief interventions that might benefit from further research.

title: The impact of prenatal alcohol exposure on social, cognitive and affective behavioral domains: Insights from rodent models.
abstract: Fetal Alcohol Spectrum Disorders (FASD) are characterized by deficits in working memory, response inhibition, and behavioral flexibility. However, the combination and severity of impairments are highly dependent upon maternal ethanol consumption patterns, which creates a complex variety of manifestations. Rodent models have been essential in identifying behavioral endpoints of prenatal alcohol exposure (PAE) However, experimental model outcomes are extremely diverse based on level, pattern, timing, and method of ethanol exposure, as well as the behavioral domain assayed and paradigm used. Therefore, comparisons across studies are difficult and there is currently no clear comprehensive behavioral phenotype of PAE. This lack of defined cognitive and behavioral phenotype is a contributing factor to the difficulty in identifying FASD individuals. The current review aims to critically examine preclinical behavioral outcomes in the social, cognitive, and affective domains in terms of the PAE paradigm, with a special emphasis on dose, timing, and delivery, to establish a working model of behavioral impairment. In addition, this review identifies gaps in our current knowledge and proposes future areas of research that will advance knowledge in the field of PAE outcomes. Understanding the complex behavioral phenotype, which results from diverse ethanol consumption will allow for development of better diagnostic tools and more critical evaluation of potential treatments for FASD.

title: Associations Between Socioeconomic Factors and Alcohol Outcomes
abstract: Socioeconomic status (SES) is one of the many factors influencing a person's alcohol use and related outcomes. Findings have indicated that people with higher SES may consume similar or greater amounts of alcohol compared with people with lower SES, although the latter group seems to bear a disproportionate burden of negative alcohol related consequences. These associations are further complicated by a variety of moderating factors, such as race, ethnicity, and gender. Thus, among individuals with lower SES, members of further marginalized communities, such as racial and ethnic minorities and homeless individuals, experience greater alcohol related consequences. Future studies are needed to more fully explore the underlying mechanisms of the relationship between SES and alcohol outcomes. This knowledge should be applied toward the development of multilevel interventions that address not only individual level risks but also economic disparities that have precipitated and maintained a disproportionate level of alcohol related consequences among more marginalized and vulnerable populations.

title: Sex and gender related differences in alcohol use and its consequences: Contemporary knowledge and future research considerations.
abstract: To review the contemporary evidence reflecting male/female differences in alcohol use and its consequences along with the biological (sex related) and psycho socio cultural (gender related) factors associated with those differences.  MEDLINE, PubMed, Web of Science, SCOPUS, PsycINFO, and CINAHL databases were searched for relevant publications, which were subsequently screened for the presence/absence of pre specified criteria for high quality evidence.  Compared to men, more women are lifetime abstainers, drink less, and are less likely to engage in problem drinking, develop alcohol related disorders or alcohol withdrawal symptoms. However, women drinking excessively develop more medical problems. Biological (sex related) factors, including differences in alcohol pharmacokinetics as well as its effect on brain function and the levels of sex hormones may contribute to some of those differences. In addition, differences in alcohol effects on behavior may also be driven by psycho socio cultural (gender related) factors. This is evident by variation in the magnitude of differences in alcohol use between countries, decreasing difference in the rates of alcohol consumption in recent generations and other findings. Evidence indicates that both sex and gender related factors are interacting with alcohol use in complex manner, which differentially impacts the risk for development of the behavioral or medical problems and alcohol use disorders in men and women.  Discovery of the mechanisms underlying biological (sex related) as well as psycho socio cultural (gender related) differences in alcohol use and related disorders is needed for development of personalized recommendations for prevention and treatment of alcohol use disorders and related problems in men and women.

title: Early adolescent patterns of alcohol, cigarettes, and marijuana polysubstance use and young adult substance use outcomes in a nationally representative sample.
abstract: Alcohol, tobacco and marijuana are the most commonly used drugs by adolescents in the U.S. However, little is known about the patterning of early adolescent substance use, and its implications for problematic involvement with substances in young adulthood. We examined patterns of substance use prior to age 16, and their associations with young adult substance use behaviors and substance use disorders in a nationally representative sample of U.S. adolescents.  Using data from Wave 4 of the Add Health Survey (n=4245) we estimated the prevalence of various patterns of early adolescent use of alcohol, cigarettes, and marijuana use individually and in combination. Then we examined the effects of patterns of early use of these substances on subsequent young adult substance use behaviors and DSM IV substance use disorders.  While 34.4% of individuals reported no substance use prior to age 16, 34.1% reported either early use of both alcohol and marijuana or alcohol, marijuana and cigarettes, indicating the relatively high prevalence of this type of polysubstance use behavior among U.S. adolescents. Early adolescent use of all three substances was most strongly associated with a spectrum of young adult substance use problems, as well as DSM IV substance use disorder diagnoses.  This research confirms the elevated prevalence and importance of polysubstance use behavior among adolescents prior to age 16, and puts early onset of alcohol, marijuana and cigarette use into the context of use patterns rather than single drug exposures.

title: Alcohol disrupts sleep homeostasis.
abstract: Alcohol is a potent somnogen and one of the most commonly used "over the counter" sleep aids. In healthy non alcoholics, acute alcohol decreases sleep latency, consolidates and increases the quality (delta power) and quantity of NREM sleep during the first half of the night. However, sleep is disrupted during the second half. Alcoholics, both during drinking periods and during abstinences, suffer from a multitude of sleep disruptions manifested by profound insomnia, excessive daytime sleepiness, and altered sleep architecture. Furthermore, subjective and objective indicators of sleep disturbances are predictors of relapse. Finally, within the USA, it is estimated that societal costs of alcohol related sleep disorders exceeds $18 billion. Thus, although alcohol associated sleep problems have significant economic and clinical consequences, very little is known about how and where alcohol acts to affect sleep. In this review, we have described our attempts to unravel the mechanism of alcohol induced sleep disruptions. We have conducted a series of experiments using two different species, rats and mice, as animal models. We performed microdialysis, immunohistochemical, pharmacological, sleep deprivation and lesion studies which suggest that the sleep promoting effects of alcohol may be mediated via alcohol's action on the mediators of sleep homeostasis: adenosine (AD) and the wake promoting cholinergic neurons of the basal forebrain (BF) Alcohol, via its action on AD uptake, increases extracellular AD resulting in the inhibition of BF wake promoting neurons. Since binge alcohol consumption is a highly prevalent pattern of alcohol consumption and disrupts sleep, we examined the effects of binge drinking on sleep wakefulness. Our results suggest that disrupted sleep homeostasis may be the primary cause of sleep disruption observed following binge drinking. Finally, we have also shown that sleep disruptions observed during acute withdrawal, are caused due to impaired sleep homeostasis. In conclusion, we suggest that alcohol may disrupt sleep homeostasis to cause sleep disruptions.

title: Intermittent ethanol access schedule in rats as a preclinical model of alcohol abuse.
abstract: One of the major challenges in preclinical studies of alcohol abuse and dependence remains the development of paradigms that will elicit high ethanol intake and mimic the progressive transition from low or moderate social drinking to excessive alcohol consumption. Exposure of outbred rats to repeated cycles of free choice ethanol intake and withdrawal with the use of intermittent access to 20% ethanol in a 2 bottle choice procedure (IA2BC) has been shown to induce a gradual escalation of voluntary ethanol intake and preference, eventually reaching ethanol consumption levels of 5 6 g/kg/24 h, and inducing pharmacologically relevant blood ethanol concentrations (BECs) This procedure has recently been gaining popularity due to its simplicity, high validity, and reliable outcomes. Here we review experimental and methodological data related to IA2BC, and discuss the usefulness and advantages of this procedure as a valuable pre training method for initiating operant ethanol self administration of high ethanol intake, as well as conditioned place preference (CPP) Despite some limitations, we provide evidence that IA2BC and related operant procedures provide the possibility to operationalize multiple aspects of alcohol abuse and addiction in a rat model, including transition from social like drinking to excessive alcohol consumption, binge drinking, alcohol seeking, relapse, and neuroadaptations related to excessive alcohol intake. Hence, IA2BC appears to be a useful and relevant procedure for preclinical evaluation of potential therapeutic approaches against alcohol abuse disorders.

title: The Alcohol Use Disorder and Associated Disabilities Interview Schedule 5 (AUDADIS 5) reliability of substance use and psychiatric disorder modules in a general population sample.
abstract: The purpose of this study was to assess the test retest reliability of substance use disorder and psychiatric modules in the Alcohol Use Disorder and Associated Disabilities Interview Schedule, Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM 5) Version (AUDADIS 5) METHODS Kappa and intraclass correlation coefficients were calculated for DSM 5 substance use and psychiatric disorder diagnoses and dimensional criteria scales using a test retest design among 1006 respondents drawn from the National Epidemiologic Survey on Alcohol and Related Conditions III (NESARC III) RESULTS Reliabilities of substance use disorder diagnoses and associated criteria scales were generally good to excellent, while reliabilities for mood, anxiety and trauma and stress related disorders and associated scales were generally in the fair to good range.  The observed reliability of the DSM 5 diagnoses and dimensional scales for the substance use and psychiatric disorders found in this study indicates that the AUDADIS 5 can be a useful tool in various research settings, particularly in studies of the general population, the target population for which it was designed.

title: Chronic Diseases and Conditions Related to Alcohol Use
abstract: Alcohol consumption is a risk factor for many chronic diseases and conditions. The average volume of alcohol consumed, consumption patterns, and quality of the alcoholic beverages consumed likely have a causal impact on the mortality and morbidity related to chronic diseases and conditions. Twenty five chronic disease and condition codes in the International Classification of Disease (ICD) 10 are entirely attributable to alcohol, and alcohol plays a component risk role in certain cancers, other tumors, neuropsychiatric conditions, and numerous cardiovascular and digestive diseases. Furthermore, alcohol has both beneficial and detrimental impacts on diabetes, ischemic stroke, and ischemic heart disease, depending on the overall volume of alcohol consumed, and, in the case of ischemic diseases, consumption patterns. However, limitations exist to the methods used to calculate the relative risks and alcohol attributable fractions. Furthermore, new studies and confounders may lead to additional diseases being causally linked to alcohol consumption, or may disprove the relationship between alcohol consumption and certain diseases that currently are considered to be causally linked. These limitations do not affect the conclusion that alcohol consumption significantly contributes to the burden of chronic diseases and conditions globally, and that this burden should be a target for intervention.