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Item The effects of alcohol odor cues on food and alcohol attentional bias, cravings, and consumption(2015-07-08) Karyadi, Kenny; Cyders, Melissa A.; Stewart, Jesse; Mosher, Catherine Esther; Grahame, Nicholas J.In order to elucidate the role of classical conditioning in food and alcohol co-consumption, the present study examined: (1) the effects of alcohol odor cues on alcohol and food cravings and attentional bias (bias in selective attention toward either food or alcohol pictures relative to neutral pictures); and (2) the role of alcohol odor cue elicited cravings and attentional biases on subsequent consumption. Participants (n = 77; mean age = 30.84, SD = 9.46; 51.9% female, 83.1% Caucasian) first completed the lab portion of the study. In this portion, they were exposed to alcohol and neutral odorants, after which their food and alcohol cravings and attentional bias were assessed. Participants then received an online survey the next day, on which they reported their level of food and alcohol consumption following the lab portion of the study. Using repeated measures analysis of covariance, alcohol odor cues were differentially effective in increasing food and alcohol attentional bias and cravings (Fs= 0.06 to 2.72, ps= 0.03 to 0.81). Using logistic and multiple regressions, alcohol odor cue elicited alcohol attentional bias, food attentional bias, and food cravings were associated with later alcohol consumption, but not with later food consumption or concurrent consumption (βs = -0.28 to 0.48, ps = 0.02 to 0.99; Exp(B)s = 0.95 to 1.83, ps = 0.33 to 0.91). Overall, alcohol odor cues can become conditioned stimuli that elicit conditioned food-related and alcohol-related responses, both of which persist long enough to motivate later alcohol consumption; however, these conditioned responses might not persist long enough to motivate later food or concurrent consumption. These findings serve as a first step in clarifying the role of classical conditioning in concurrent consumption. In particular, they suggest that additional empirical investigations are needed to: (1) clarify the classical conditioning mechanisms underlying concurrent consumption; and (2) examine whether interventions targeting classical conditioning mechanisms are effective for reducing alcohol use.Item Evidence of causal effect of major depression on alcohol dependence: findings from the psychiatric genomics consortium(Cambridge University Press, 2019-05) Polimanti, Renato; Peterson, Roseann E.; Ong, Jue-Sheng; MacGregor, Stuart; Edwards, Alexis C.; Clarke, Toni-Kim; Frank, Josef; Gerring, Zachary; Gillespie, Nathan A.; Lind, Penelope A.; Maes, Hermine H.; Martin, Nicholas G.; Mbarek, Hamdi; Medland, Sarah E.; Streit, Fabian; Agrawal, Arpana; Edenberg, Howard J.; Kendler, Kenneth S.; Lewis, Cathryn M.; Sullivan, Patrick F.; Wray, Naomi R.; Gelernter, Joel; Derks, Eske M.; Biochemistry and Molecular Biology, School of MedicineBACKGROUND: Despite established clinical associations among major depression (MD), alcohol dependence (AD), and alcohol consumption (AC), the nature of the causal relationship between them is not completely understood. We leveraged genome-wide data from the Psychiatric Genomics Consortium (PGC) and UK Biobank to test for the presence of shared genetic mechanisms and causal relationships among MD, AD, and AC. METHODS: Linkage disequilibrium score regression and Mendelian randomization (MR) were performed using genome-wide data from the PGC (MD: 135 458 cases and 344 901 controls; AD: 10 206 cases and 28 480 controls) and UK Biobank (AC-frequency: 438 308 individuals; AC-quantity: 307 098 individuals). RESULTS: Positive genetic correlation was observed between MD and AD (rgMD-AD = + 0.47, P = 6.6 × 10-10). AC-quantity showed positive genetic correlation with both AD (rgAD-AC quantity = + 0.75, P = 1.8 × 10-14) and MD (rgMD-AC quantity = + 0.14, P = 2.9 × 10-7), while there was negative correlation of AC-frequency with MD (rgMD-AC frequency = -0.17, P = 1.5 × 10-10) and a non-significant result with AD. MR analyses confirmed the presence of pleiotropy among these four traits. However, the MD-AD results reflect a mediated-pleiotropy mechanism (i.e. causal relationship) with an effect of MD on AD (beta = 0.28, P = 1.29 × 10-6). There was no evidence for reverse causation. CONCLUSION: This study supports a causal role for genetic liability of MD on AD based on genetic datasets including thousands of individuals. Understanding mechanisms underlying MD-AD comorbidity addresses important public health concerns and has the potential to facilitate prevention and intervention efforts.Item The Impact of Social Media on Social Behaviors and Alcohol Consumption(2016-04-08) Burress, KimberlyThis research project examines the subliminal effects that alcohol consumption may or may not have on a person’s technology-based social behaviors. If the effect of alcohol consumption alters social behaviors, then a logical question is whether and how these behaviors are expressed through social media. Sub-areas of inquiry include alcohol’s effect on mood, alcohol-based interactions on social media and the impact of alcohol on an individual’s use of different social media platforms. The main objective of this research is to obtain a clearer understanding of the extent to which alcohol consumption and advertisement impact social media interactions. If correlations can be found, then a further step is to examine alcohol consumption interactions and advertising-based interactions and their influence on the activities of other social media users and the content of their posts. The research will examine social media content created about consuming alcohol through the use of keyword analysis. It will focus specifically on data that can be gleaned from Facebook and Twitter postings. The frequency of social media content creation when under the influence of alcohol will be compared with content creation during periods of sobriety. The research will discern whether there is a noticeable change in content subject matter, attitude and/or tone when alcohol is being consumed. It will also determine whether there is a correlation between social media advertisements related to alcohol, and if so, whether the followers of those advertisements increase their own alcohol-related user content and whether this then increases alcohol consumption. Technology such as social media has significantly reduced the time and distance between communication channels and users. This research project examines technology-based social behaviors to discern whether user content on social media can be collected and analyzed to cultivate additional sales within the alcohol industry.Item Interaction between the patatin-like phospholipase domain-containing protein 3 genotype and coffee drinking and the risk for acute alcoholic hepatitis(Wiley, 2017-11-11) Liangpunsakul, Suthat; Beaudoin, James J.; Shah, Vijay H.; Puri, Puneet; Sanyal, Arun J.; Kamath, Patrick S.; Lourens, Spencer G.; Tang, Qing; Katz, Barry P.; Crabb, David W.; Chalasani, Naga P.; Medicine, School of MedicineOnly a subset of subjects with excessive alcohol consumption develops alcoholic liver disease (ALD). One of the major risk factors for ALD is the genetic variant of the patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene. Coffee is one of the most commonly consumed beverages, and coffee consumption has been associated with lower levels of serum alanine aminotransferase. The aim of this study was to investigate the role of coffee drinking and PNPLA3 rs738409 and their association with alcoholic hepatitis (AH) in a well-characterized cohort of subjects from the Translational Research and Evolving Alcoholic Hepatitis Treatment consortium. AH subjects and heavy drinking controls without a history of liver disease who were enrolled between May 2013 and May 2016 were included (n = 339), and the details of alcohol and coffee consumption were assessed. The PNPLA3 variant was determined among participants of European ancestry (n = 183). Relationships between baseline data and AH status were determined, and multivariable logistic regression modeling was performed. During the study period, 189 cases with AH and 150 heavy drinking controls were prospectively enrolled. The prevalence of regular coffee consumption was significantly lower in patients with AH compared to controls (20% versus 43%; P < 0.0001). The overall minor allele frequency of the PNPLA3 variant was higher in AH cases. Multivariable logistic regression revealed that coffee consumption and PNPLA3 were significantly associated with AH status at baseline after adjusting for relevant patient characteristics. Conclusion: We found a higher prevalence of AH among heavy drinkers with PNPLA3 G/G and G/C genotypes regardless of coffee consumption status and a higher prevalence of AH among heavy drinkers who were not regular coffee drinkers. These findings remained after considering relevant baseline patient characteristics. Further studies are needed to confirm our observation.Item Prohibition of e-cigarettes in the US: Are prohibitions where alcohol is consumed related to lower alcohol consumption?(Palgrave Macmillan, 2016-12) Hershberger, Alexandra R.; Karyadi, Kenny A.; Cyders, Melissa A.; Psychology, School of ScienceRecently, research has suggested negative consequences related to electronic cigarette (e-cig) use, including the increased risk for alcohol use and abuse. Previous work found that cigarette smoking ban legislation lowered overall smoking and alcohol use rates; however, researchers have not yet examined the potential effects of prohibiting e-cig use. The present study surveyed 617 individuals from a community-based online sample in the US (mean age = 33.33, SD = 10.50, 54.7 per cent female) who reported their smoking/e-cig use status, alcohol consumption, and the presence of e-cig prohibitions where they consume alcohol. E-cig prohibition was associated with a lower likelihood of being an e-cig user (OR = 0.12, p < 0.001) or dual user (use both cigarettes and e-cigs) (OR = 0.07, p < 0.001). Alcohol Use Disorder Identification Test scores (b = -1.92, p < 0.001), total drinks consumed over 14 days (b = -4.58, p = 0.002), and average drinks per drinking day (b = -0.71, p < 0.001) were all lower when e-cigs were prohibited. Findings are an initial step in this line of research and suggest important future work examining implications of e-cig prohibition recommendations and policy.Item The sequenced rat brain transcriptome--its use in identifying networks predisposing alcohol consumption(Wiley, 2015-09) Saba, Laura M.; Flink, Stephen C.; Vanderlinden, Lauren A.; Israel, Yedy; Tampier, Lutske; Colombo, Giancarlo; Kiianmaa, Kalervo; Bell, Richard L.; Printz, Morton P.; Flodman, Pamela; Koob, George; Richardson, Heather N.; Lombardo, Joseph; Hoffman, Paula L.; Tabakoff, Boris; Department of Psychiatry, IU School of MedicineA quantitative genetic approach, which involves correlation of transcriptional networks with the phenotype in a recombinant inbred (RI) population and in selectively bred lines of rats, and determination of coinciding QTLs for gene expression and the trait of interest, has been applied in the current study. In this analysis, a novel approach was used that combined DNA-Seq data, data from brain exon array analysis of HXB/BXH RI rat strains and six pairs of rat lines selectively bred for high and low alcohol preference, and RNA-Seq data (including rat brain transcriptome reconstruction) to quantify transcript expression levels, generate co-expression modules, and identify biological functions that contribute to the predisposition to consume varying amounts of alcohol. A gene co-expression module was identified in the RI rat strains that contained both annotated and unannotated transcripts expressed in brain, and was associated with alcohol consumption in the RI panel. This module was found to be enriched with differentially expressed genes from the selected lines of rats. The candidate genes within the module and differentially expressed genes between high and low drinking selected lines were associated with glia (microglia and astrocytes), and could be categorized as being related to immune function, energy metabolism and calcium homeostasis, and glial-neuronal communication. Our results illustrate that there are multiple combinations of genetic factors that can produce the same phenotypic outcome. While no single gene accounts for predisposition to a particular level of alcohol consumption in every animal model, coordinated differential expression of subsets of genes in the identified pathways produce similar phenotypic outcomes.