Factors influencing COVID-19 Infection in older individuals: History of Alcohol Use Disorder, Major Depressive illness, genetic variation and current use of alcohol.
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SUBMITTER: Hill SY
PROVIDER: S-EPMC8669850 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:IntroductionSmoking among adults with major depressive disorder (MDD) is at least double that of the general US population. More effective smoking cessation interventions for depressed smokers may be facilitated through a better understanding of the smoking and depression-related characteristics of this population.MethodsWe used baseline data from 300 participants enrolled in randomized clinical trial for smokers with current or past MDD. We described history of smoking cessation behaviors (ie, quit attempts, quit motivation, and cessation treatment utilization) and used multivariate regression to identify demographic and depression-related correlates of these behaviors.ResultsSixty-eight percent of participants reported at least one quit attempt in the past year, nearly 51% reported motivation to quit in the subsequent 30 days, and 83% reported prior use of a nicotine replacement therapy. A greater readiness to quit smoking was associated with increased age (p = .04) and lower cigarettes per day (p = .01). Greater use of smoking cessation medication was associated with greater education and nicotine dependence, minority race, and greater use of complementary reinforcers (eg, activities associated with increased reinforcing value of smoking; p's < .05).ConclusionsThese data indicate that smokers with current or past MDD are highly motivated to quit smoking and have a history of engaging in efforts to quit. Interventions to promote smoking cessation behaviors should address younger and lighter smokers, who may perceive less risk from tobacco use, and efforts to promote smoking cessation medications and counseling should address minority smokers who are engaging in complementary reinforcers.ImplicationsThese data are inconsistent with the assumption that smokers with serious mental illness are not willing to quit smoking and suggest the need for studies that test behavioral interventions that address complementary reinforcers to treat tobacco use in this community.
| S-EPMC8666119 | biostudies-literature
Project description:BackgroundRacial discrimination has consistently been linked to elevated alcohol use and smoking in Black adults, but the independent contributions of everyday and major experiences of discrimination have rarely been investigated. The present study aimed to identify variation in magnitude of the links between each type of racial discrimination with current frequency of alcohol use and regular smoking by demographic characteristics and family history of problem drinking/regular smoking in Black adults in the U.S.MethodsData were drawn from 4462 adults (29.40% Afro Caribbean, 70.60% African American; 63.20% female) in a nationally representative sample of Black Americans. Logistic regression analyses were conducted to predict current frequency of alcohol use and regular smoking using the Everyday Discrimination Scale (EDS) and Major Experiences of Discrimination Scale (MEDS), testing for interactions with demographic characteristics and family history.ResultsIn the alcohol model, an EDS by education level interaction was observed: OR = 1.04 (CI:1.02-1.07) for < high school; OR = 0.95 (CI:0.92-0.98) for ≥ high school. MEDS was independently associated with alcohol use (OR = 1.11, CI:1.04-1.18). In the smoking model, EDS was associated with elevated risk (OR = 1.03, CI:1.01-1.04) and a MEDS by age cohort interaction was observed: OR = 1.24 (CI:1.11-1.38) for <age 45; OR = 1.07 (CI:0.97-1.19) for ages 45-65.ConclusionsEveryday and major experiences of racial discrimination contribute independently to both alcohol use and regular smoking in Black adults, with some variation by education level and age. Differentiating everyday from major experiences of discrimination in studies of mechanisms linking racial discrimination to substance use will enhance their informativeness for intervention development.
| S-EPMC7894990 | biostudies-literature
Project description:BackgroundDepressive symptoms are common among individuals with alcohol use disorders and impact treatment outcome. Substantial overlap exists among the neurobiological systems proposed in the pathophysiology of depressive and alcohol use disorders; however, specific genetic effects contributing to risk for depressive comorbidity remain poorly understood.MethodsThis study examines the association of depressive symptom scores for lifetime depression (the sum of DSM-IV major depression co-endorsed criteria for lifetime depression) with markers in 120 candidate genes in 554 alcohol-dependent individuals. The candidate genes code for molecules involved in dopamine, serotonin, glutamate, gamma-aminobutyric acid (GABA), and opioid neurotransmission, cell signaling, pharmacokinetics, stress biology, and behavioral control. Analyses were conducted at the single marker level with experimentwise permutation to control for multiple testing.ResultsResults revealed nominal associations for markers in 20 genes. Following experimentwise permutation, markers in the corticotropin-releasing hormone-binding protein (CRHBP) the μ-opioid receptor (OPRM1) and the β1 subunit of GABA A (GABA(A)) receptors (GABRB1) met or exceeded the significance threshold. None of the markers associated with depressive symptom scores were significantly associated with alcohol dependence symptom scores.ConclusionThese findings suggest potential risk genes for depressive symptoms in alcohol-dependent individuals.
| S-EPMC3116055 | biostudies-literature
Project description:OBJECTIVE:The purpose of this study was to update estimates of comorbidity between lifetime alcohol use disorder (AUD) severity and lifetime major depressive disorder (MDD) in San Juan, Puerto Rico. METHOD:Data are from a household random sample of 1,510 individuals (816 female) 18-64 years of age in San Juan, Puerto Rico. AUD and MDD identification follow criteria from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition and Fourth Edition, respectively, both implemented with the Composite International Diagnostic Interview (CIDI). It is possible to implement DSM-5 AUD identification with the CIDI, but only DSM-IV criteria can be applied to identify MDD. RESULTS:The prevalence of lifetime MDD was 11% among men, 17% among women, and 14% for both genders; the prevalence of lifetime AUD was 38% among men, 16% among women, and 26% for both genders. Among those with AUD, the rate of MDD was 17% among men and 35% among women. Among those without AUD the rate of MDD was 7% among men and 15% among women. Results of multiple logistic regression analysis controlling for gender, illegal drug use, age, level of family cohesion, religion, employment status, marital status, education, and family annual income showed that AUD severity was positively associated with the likelihood of MDD, as follows: mild AUD, adjusted odds ratio [AOR] = 1.78 (95% CI [1.09, 2.91], p < .05); moderate AUD, AOR = 2.58 (95% CI [1.33, 5.01], p < .01); and severe AUD, AOR = 3.34 (95% CI [1.70, 6.56], p < .01). CONCLUSIONS:MDD frequently occurs as a comorbid condition with AUD in San Juan, Puerto Rico. The frequency of occurrence increases as AUD severity increases. AUD treatment providers should therefore be equally prepared to treat these two comorbid conditions.
| S-EPMC6811725 | biostudies-literature
Project description:Despite converging evidence that major depressive illness is associated with both memory impairment and hippocampal pathology, findings vary widely across studies and it is not known whether these changes are regionally specific. In the present study we acquired brain MRIs (magnetic resonance images) from 31 unmedicated patients with MDD (major depressive disorder; mean age 39.2+/-11.9 years; 77% female) and 31 demographically comparable controls. Three-dimensional parametric mesh models were created to examine localized alterations of hippocampal morphology. Although global volumes did not differ between groups, statistical mapping results revealed that in MDD patients, more severe depressive symptoms were associated with greater left hippocampal atrophy, particularly in CA1 (cornu ammonis 1) subfields and the subiculum. However, previous treatment with atypical antipsychotics was associated with a trend towards larger left hippocampal volume. Our findings suggest effects of illness severity on hippocampal size, as well as a possible effect of past history of atypical antipsychotic treatment, which may reflect prolonged neuroprotective effects. This possibility awaits confirmation in longitudinal studies.
| S-EPMC2785515 | biostudies-literature
Project description:Reward-based reinforcement learning impairments are common in major depressive disorder, but it is unclear which aspects of reward-based reinforcement learning are disrupted in remitted major depression (rMDD). Given that the neurobiological substrates that implement reward-based RL are also strongly implicated in psychomotor retardation (PmR), the present study sought to test whether reward-based reinforcement learning is altered in rMDD individuals with a history of PmR. Three groups of individuals (1) rMDD with past PmR (PmR+, N = 34), (2) rMDD without past PmR (PmR-, N = 44), and (3) healthy controls (N = 90) completed a reward-based reinforcement learning task. Computational modeling was applied to test for group differences in model-derived parameters - specifically, learning rates and reward sensitivity. Compared to controls, rMDD PmR + exhibited lower learning rates, but not reduced reward sensitivity. By contrast, rMDD PmR- did not significantly differ from controls on either of the model-derived parameters. Follow-up analyses indicated that the results were not due to current psychopathology symptoms. Results indicate that a history of PmR predicts altered reward-based reinforcement learning in rMDD. Abnormal reward-related reinforcement learning may reflect a scar of past depressive episodes that contained psychomotor symptoms, or a trait-like deficit that preceded these episodes.
| S-EPMC10185002 | biostudies-literature
Project description:Alcohol consumption is typically correlated with the alcohol use behaviors of one's peers. Previous research has suggested that this positive relationship could be due to social selection, social influence, or a combination of both processes. However, few studies have considered the role of shared genetic and environmental influences in conjunction with causal processes.This study uses data from a sample of male twins (N = 1,790) who provided retrospective reports of their own alcohol consumption and their peers' alcohol-related behaviors, from adolescence into young adulthood (ages 12 to 25). Structural equation modeling was employed to compare 3 plausible models of genetic and environmental influences on the relationship between phenotypes over time.Model fitting indicated that one's own alcohol consumption and the alcohol use of one's peers are related through both genetic and shared environmental factors and through unique environmental causal influences. The relative magnitude of these factors, and their contribution to covariation, changed over time, with genetic factors becoming more meaningful later in development.Peers' alcohol use behaviors and one's own alcohol consumption are related through a complex combination of genetic and environmental factors that act via correlated factors and the complementary causal mechanisms of social selection and influence. Understanding these processes can inform risk assessment as well as improve our ability to model the development of alcohol use.
| S-EPMC4331262 | biostudies-other
Project description:The purpose of this review is to examine human and preclinical data that are relevant to the following hypotheses. The first hypothesis is that deficient CB1R-mediated signaling results in symptoms that mimic those seen in depression. The second hypothesis is that activation of CB1R-mediated signaling results in behavioral, endocrine and other effects that are similar to those produced by currently used antidepressants. The third hypothesis is that conventional antidepressant therapies act through enhanced CB1R mediated signaling. Together the available data indicate that activators of CB1R signaling, particularly inhibitors of fatty acid amide hydrolase, should be considered for clinical trials for the treatment of depression.
| S-EPMC4002665 | biostudies-literature
Project description:The co-occurrence of HIV and alcohol use disorder (AUD) amplifies risk for neural injury and neurocognitive deficits. However, the substantial neurocognitive heterogeneity across HIV+/AUD+ individuals suggests inter-individual differences in vulnerability to the neurotoxicity of comorbid HIV/AUD. Genetic variation in alcohol dehydrogenase (ADH), which metabolizes ethanol, may contribute to inter-individual neurocognitive variability. We evaluated associations between five ADH single-nucleotide polymorphisms (SNPs) and neurocognition in men stratified by HIV and lifetime AUD status. Neurobehavioral assessments were administered to 153 men. Three-way ANOVAs examined the interaction of HIV, AUD, and ADH SNPs on global and domain-specific demographically corrected T scores. Follow-up ANCOVAs adjusted for age, estimated verbal IQ, depression, and remote non-alcohol substance use disorders. HIV/AUD groups differed globally and for verbal fluency, working memory, executive function, and processing speed T scores specifically, with HIV+/AUD+ exhibiting the poorest performance. ADH4 (rs1126671) was associated with large effects on working memory (d = - 1.16, p = .001) and executive function (d = - 0.77, p = .028) selectively in HIV+/AUD+, which remained significant in ANCOVA models. ADH1A (rs3819197) moderated the deleterious effects of HIV+/AUD+ on processing speed such that HIV+/AUD+ related to slower information processing in A allele carriers but not GG homozygotes (ps < 0.03). Preliminary findings suggest genetic variation in the ADH pathway moderates the deleterious neurocognitive effects of comorbid HIV/AUD. Differential metabolism of heavy ethanol exposure may compromise neurocognition under conditions of neurobiological stress, such as in HIV infection. The functional effects on ethanol metabolism of ADH SNPs examined in this study remain poorly understood, warranting further examination of pharmacokinetic mechanisms mediating ADH gene-neurobehavior relationships in HIV.
| S-EPMC7261244 | biostudies-literature
Project description:Major depressive disorder (MDD) is a common, complex psychiatric disorder and a leading cause of disability worldwide. Despite twin studies indicating its modest heritability (~30-40%), extensive heterogeneity and a complex genetic architecture have complicated efforts to detect associated genetic risk variants. We combined single-nucleotide polymorphism (SNP) summary statistics from the CONVERGE and PGC studies of MDD, representing 10 502 Chinese (5282 cases and 5220 controls) and 18 663 European (9447 cases and 9215 controls) subjects. We determined the fraction of SNPs displaying consistent directions of effect, assessed the significance of polygenic risk scores and estimated the genetic correlation of MDD across ancestries. Subsequent trans-ancestry meta-analyses combined SNP-level evidence of association. Sign tests and polygenic score profiling weakly support an overlap of SNP effects between East Asian and European populations. We estimated the trans-ancestry genetic correlation of lifetime MDD as 0.33; female-only and recurrent MDD yielded estimates of 0.40 and 0.41, respectively. Common variants downstream of GPHN achieved genome-wide significance by Bayesian trans-ancestry meta-analysis (rs9323497; log10 Bayes Factor=8.08) but failed to replicate in an independent European sample (P=0.911). Gene-set enrichment analyses indicate enrichment of genes involved in neuronal development and axonal trafficking. We successfully demonstrate a partially shared polygenic basis of MDD in East Asian and European populations. Taken together, these findings support a complex etiology for MDD and possible population differences in predisposing genetic factors, with important implications for future genetic studies.
| S-EPMC5404611 | biostudies-literature