Browsing by Subject "Alcohol consumption"
Now showing 1 - 10 of 15
Results Per Page
Sort Options
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 From detection to intervention, optimizing care for patients with alcohol use disorder and advanced hepatic fibrosis(Wiley, 2024) Zuluaga, Paola; Liangpunsakul, Suthat; Medicine, School of MedicineItem Functional 3’-UTR Variants Identify Regulatory Mechanisms Impacting Alcohol Use Disorder and Related Traits(bioRxiv, 2024-02-05) Chen, Andy B.; Yu, Xuhong; Thapa, Kriti S.; Gao, Hongyu; Reiter, Jill L.; Xuei, Xiaoling; Tsai, Andy P.; Landreth, Gary E.; Lai, Dongbing; Wang, Yue; Foroud, Tatiana M.; Tischfield, Jay A.; Edenberg, Howard J.; Liu, Yunlong; Medical and Molecular Genetics, School of MedicineAlthough genome-wide association studies (GWAS) have identified loci associated with alcohol consumption and alcohol use disorder (AUD), they do not identify which variants are functional. To approach this, we evaluated the impact of variants in 3' untranslated regions (3'-UTRs) of genes in loci associated with substance use and neurological disorders using a massively parallel reporter assay (MPRA) in neuroblastoma and microglia cells. Functionally impactful variants explained a higher proportion of heritability of alcohol traits than non-functional variants. We identified genes whose 3'UTR activities are associated with AUD and alcohol consumption by combining variant effects from MPRA with GWAS results. We examined their effects by evaluating gene expression after CRISPR inhibition of neuronal cells and stratifying brain tissue samples by MPRA-derived 3'-UTR activity. A pathway analysis of differentially expressed genes identified inflammation response pathways. These analyses suggest that variation in response to inflammation contributes to the propensity to increase alcohol consumption.Item Genes identified in rodent studies of alcohol intake are enriched for heritability of human substance use(Wiley, 2021) Huggett, Spencer B.; Johnson, Emma C.; Hatoum, Alexander S.; Lai, Dongbing; Srijeyanthan, Jenani; Bubier, Jason A.; Chesler, Elissa J.; Agrawal, Arpana; Palmer, Abraham A.; Edenberg, Howard J.; Palmer, Rohan H. C.; Medical and Molecular Genetics, School of MedicineBackground: Rodent paradigms and human genome-wide association studies (GWAS) on drug use have the potential to provide biological insight into the pathophysiology of addiction. Methods: Using GeneWeaver, we created rodent alcohol and nicotine gene-sets derived from 19 gene expression studies on alcohol and nicotine outcomes. We partitioned the SNP heritability of these gene-sets using four large human GWAS: (1) alcoholic drinks per week, (2) problematic alcohol use, (3) cigarettes per day, and (4) smoking cessation. We benchmarked our findings with curated human alcohol and nicotine addiction gene-sets and performed specificity analyses using other rodent gene-sets (e.g., locomotor behavior) and other human GWAS (e.g., height). Results: The rodent alcohol gene-set was enriched for heritability of drinks per week, cigarettes per day, and smoking cessation, but not problematic alcohol use. However, the rodent nicotine gene-set was not significantly associated with any of these traits. Both rodent gene-sets showed enrichment for several non-substance-use GWAS, and the extent of this relationship tended to increase as a function of trait heritability. In general, larger gene-sets demonstrated more significant enrichment. Finally, when evaluating human traits with similar heritabilities, both rodent gene-sets showed greater enrichment for substance use traits. Conclusion: Our results suggest that rodent gene expression studies can help to identify genes that contribute to the heritability of some substance use traits in humans, yet there was less specificity than expected. We outline various limitations, interpretations, and considerations for future research.Item A Genome Wide Association Study of Interhemispheric Theta EEG Coherence: Implications for Neural Connectivity and Alcohol Use Behavior(Springer Nature, 2021) Meyers, Jacquelyn L.; Zhang, Jian; Chorlian, David B.; Pandey, Ashwini K.; Kamarajan, Chella; Wang, Jen-Chyong; Wetherill, Leah; Lai, Dongbing; Chao, Michael; Chan, Grace; Kinreich, Sivan; Kapoor, Manav; Bertelsen, Sarah; McClintick, Jeanette; Bauer, Lance; Hesselbrock, Victor; Kuperman, Samuel; Kramer, John; Salvatore, Jessica E.; Dick, Danielle M.; Agrawal, Arpana; Foroud, Tatiana; Edenberg, Howard J.; Goate, Alison; Porjesz, Bernice; Medical and Molecular Genetics, School of MedicineAberrant connectivity of large-scale brain networks has been observed among individuals with alcohol use disorders (AUDs) as well as in those at risk, suggesting deficits in neural communication between brain regions in the liability to develop AUD. Electroencephalographical (EEG) coherence, which measures the degree of synchrony between brain regions, may be a useful measure of connectivity patterns in neural networks for studying the genetics of AUD. In 8810 individuals (6644 of European and 2166 of African ancestry) from the Collaborative Study on the Genetics of Alcoholism (COGA), we performed a Multi-Trait Analyses of genome-wide association studies (MTAG) on parietal resting-state theta (3-7 Hz) EEG coherence, which previously have been associated with AUD. We also examined developmental effects of GWAS findings on trajectories of neural connectivity in a longitudinal subsample of 2316 adolescent/young adult offspring from COGA families (ages 12-30) and examined the functional and clinical significance of GWAS variants. Six correlated single nucleotide polymorphisms located in a brain-expressed lincRNA (ENSG00000266213) on chromosome 18q23 were associated with posterior interhemispheric low theta EEG coherence (3-5 Hz). These same variants were also associated with alcohol use behavior and posterior corpus callosum volume, both in a subset of COGA and in the UK Biobank. Analyses in the subsample of COGA offspring indicated that the association of rs12954372 with low theta EEG coherence occurred only in females, most prominently between ages 25 and 30 (p < 2 × 10-9). Converging data provide support for the role of genetic variants on chromosome 18q23 in regulating neural connectivity and alcohol use behavior, potentially via dysregulated myelination. While findings were less robust, genome-wide associations were also observed with rs151174000 and parieto-frontal low theta coherence, rs14429078 and parieto-occipital interhemispheric high theta coherence, and rs116445911 with centro-parietal low theta coherence. These novel genetic findings highlight the utility of the endophenotype approach in enhancing our understanding of mechanisms underlying addiction susceptibility.Item Impact of low alcohol consumption in the natural history of cirrhosis(AME, 2024) Marti-Aguado, David; Vilar-Gomez, Eduardo; Medicine, School of MedicineItem 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 Item-Level Genome-Wide Association Study of the Alcohol Use Disorders Identification Test in Three Population-Based Cohorts(American Psychiatric Association, 2022) Mallard, Travis T.; Savage, Jeanne E.; Johnson, Emma C.; Huang, Yuye; Edwards, Alexis C.; Hottenga, Jouke J.; Grotzinger, Andrew D.; Gustavson, Daniel E.; Jennings, Mariela V.; Anokhin, Andrey; Dick, Danielle M.; Edenberg, Howard J.; Kramer, John R.; Lai, Dongbing; Meyers, Jacquelyn L.; Pandey, Ashwini K.; Harden, Kathryn Paige; Nivard, Michel G.; de Geus, Eco J. C.; Boomsma, Dorret I.; Agrawal, Arpana; Davis, Lea K.; Clarke, Toni-Kim; Palmer, Abraham A.; Sanchez-Roige, Sandra; Biochemistry and Molecular Biology, School of MedicineObjective: Genome-wide association studies (GWASs) of the Alcohol Use Disorders Identification Test (AUDIT), a 10-item screen for alcohol use disorder (AUD), have elucidated novel loci for alcohol consumption and misuse. However, these studies also revealed that GWASs can be influenced by numerous biases (e.g., measurement error, selection bias), which may have led to inconsistent genetic correlations between alcohol involvement and AUD, as well as paradoxically negative genetic correlations between alcohol involvement and psychiatric disorders and/or medical conditions. The authors used genomic structural equation modeling to elucidate the genetics of alcohol consumption and problematic consequences of alcohol use as measured by AUDIT. Methods: To explore these unexpected differences in genetic correlations, the authors conducted the first item-level and the largest GWAS of AUDIT items (N=160,824) and applied a multivariate framework to mitigate previous biases. Results: The authors identified novel patterns of similarity (and dissimilarity) among the AUDIT items and found evidence of a correlated two-factor structure at the genetic level ("consumption" and "problems," rg=0.80). Moreover, by applying empirically derived weights to each of the AUDIT items, the authors constructed an aggregate measure of alcohol consumption that was strongly associated with alcohol dependence (rg=0.67), moderately associated with several other psychiatric disorders, and no longer positively associated with health and positive socioeconomic outcomes. Lastly, by conducting polygenic analyses in three independent cohorts that differed in their ascertainment and prevalence of AUD, the authors identified novel genetic associations between alcohol consumption, alcohol misuse, and health. Conclusions: This work further emphasizes the value of AUDIT for both clinical and genetic studies of AUD and the importance of using multivariate methods to study genetic associations that are more closely related to AUD.